Types of necrosis. Causes of tissue necrosis. General treatment of wet necrosis

By its nature, the disease in question has quite serious consequences, since the result of necrosis is the death of individual (sometimes very large) areas of tissue. As a result, the patient’s organs and systems will not be able to function fully in the future. Necrosis is often the cause of death: pathological cells grow very quickly, so you should respond to the first symptoms of the disease immediately.

Diagnosis of necrosis - how to determine the form and stage of the disease?

In its development, this disease goes through 3 stages:

• Pre-necrosis.

On at this stage certain changes take place, but they are reversible.

• Death of tissues.

Necrosis of the affected cells occurs.

• Destructive changes.

Pathological tissues disintegrate.

To identify necrosis that is superficial in nature, special problems does not arise: the doctor familiarizes himself with the patient’s complaints, conducts blood testing, and takes a sample of fluid from the wound surface. In some cases, if there is a suspicion of gas gangrene, an x-ray of the affected area may be prescribed (to confirm the presence of gases).

With necrosis internal organs The diagnostic procedure is more extensive and may include:

• Ren tgenography.

Effective at stages 2 and 3 of the disease. At the initial stage of the disease, even in the presence of pronounced manifestations, the disease may not be detected. With sequestration, the problems of diagnosing late stages may lie in the fact that this pathology will be combined with osteoporosis, which is endowed with similar symptoms

• Radioisotope scanning.

It is prescribed in cases where the previous diagnostic method was unsuccessful. To carry out this procedure, the patient is given medical drug, which contains a radioactive substance. A few hours later, zones of radioactivity are detected in the patient’s body. The area affected by necrosis, due to the lack of blood circulation in it, will be presented in the image as a “cold” spot.

• Computed tomography.

Used at all stages, if bone necrosis is suspected. At an early stage of the development of this pathology, the diagnostician, when performing a CT scan, should pay attention to the presence of cystic cavities filled with fluid. The presence of such formations, when previous research methods are unfruitful; The patient's complaints will help determine the diagnosis.

• Magnetic resonance imaging.

Effective at any stage of the disease, painless, safe for the patient. Using this research method, it is possible to detect even minor errors that are associated with impaired blood circulation in the tissues of internal organs.

Treatment methods for necrosis

How is surgery performed for necrosis?

Surgical treatment for necrosis is not indicated in all cases: everything will depend on the form of necrosis and its stage:

• Necrotomy.

It is used for wet necrosis (wet gangrene), which is localized in the area of ​​the extremities and chest. Resection of pathological tissue is often performed without the use of anesthesia. The depth of the incision should reach healthy tissue until bleeding begins.

Indicated for wet necrosis, within the framework of non-dead tissue. The signal for carrying out this manipulation is the appearance of a clear boundary, which separates healthy tissue from pathological tissue.

After noncreatomy, dermatoplasty should be performed, or (if the defective tissue is not too large in volume) sutures should be applied.

• Amputation of a limb/resection of the affected organ. Required under the following circumstances:

1. The patient is diagnosed with wet necrosis (wet gangrene), which is rapidly progressing.
2. There is dry necrosis that does not respond to conservative treatment, there are signs of its transition to wet necrosis.

When amputating a limb, resection is carried out significantly above the visible level of the lesion. The length of hospital stay after amputation is completed can vary from 6 to 14 days. IN postoperative period the patient must take a course of antibiotics and painkillers. If there are no complications after the manipulation, prosthetics can be performed after 2 weeks.

Amputation due to necrosis is fraught with the following complications:

• Necrosis of the skin in the stump area. This phenomenon can occur when there is an inadequate blood supply to the tissues of the specified area.
• Angiotrophoneurosis. A consequence of a violation of the integrity of the nerves during manipulation. In the future, the person operated on will complain of pain in the scar area.
• Phantom pain. For some time after the operation, the patient may have pain or an itch in the amputated limb.
• Keloid scars. They are postoperative scars of considerable size. Their formation is associated with the predisposition of the person operated on to such phenomena.

For necrosis that affects bone tissue, several types of surgical procedures can be used:

Endoprosthetics

Provides for replacing the affected joint with an artificial one. The implant must be made of durable materials (titanium, zirconium). The pin is fixed using cement/glue. Endoprosthesis replacement is a common operation for bone lesions among patients over 50 years of age. The procedure in question is quite complicated to perform. Among postoperative complications the most popular are: infection, loosely fixed prosthesis (needs re-operation).

Arthrodesis

This manipulation involves resection of bones that articulate with each other. After this, these bones are connected, thereby ensuring their fusion in the future. This procedure is fraught with negative consequences in terms of the patient’s ability to work: it is problematic to climb/descend stairs and sit.

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Necrosis(from Greek nekros- dead) - necrosis, death of cells and tissues in a living organism; At the same time, their vital activity ceases completely. The necrotic process goes through a number of stages, which allows us to talk about morphogenesis necrosis: 1) paranecrosis - similar to necrotic, but reversible changes; 2) necrobiosis - irreversible dystrophic changes characterized by a predominance of catabolic reactions over anabolic ones; 3) cell death, the time of which is difficult to determine; 4) autolysis - decomposition of a dead substrate under the action of hydrolytic enzymes of dead cells and macrophages. In morphological terms, necrosis is equivalent to autolysis. A peculiar form of necrosis is apoptosis(from Greek aro - division and ptosis- omission, fall). Apoptosis is based on the division of a cell into parts with the formation of apoptotic bodies (cell fragments surrounded by a membrane and capable of vital activity) and the subsequent phagocytosis of these bodies by macrophages.

Necrobiotic and necrotic processes (necrosis, apoptosis) occur constantly as a manifestation normal life the body, since the performance of any function requires the expenditure of a material substrate, which is replenished by physiological regeneration. In addition, most of the body's cells are constantly subject to aging, natural death, followed by their destruction through apoptosis and physiological autolysis.

Thus, processes of physiological destruction are constantly occurring in the body, i.e. necrotic, autolytic and restorative, i.e. reparative, regenerative processes, which ensures its normal functioning.

Necrosis occurs more often and earlier in functionally active parenchymal structures (functionally burdened parts of the myocardium, proximal and distal parts of the kidneys, neurons of the brain, etc.). Necrosis can affect a part of a cell, a cell, a group of cells, a section of tissue, an organ, an entire organ, or a part of the body. Therefore, in some cases it is determined only when microscopic examination, in others - clearly visible to the naked eye.

Microscopic signs of necrosis. These include characteristic cell changes and intercellular substance. Cell changes concern both the nucleus and the cytoplasm. The kernel shrinks, while

chromatin condensation occurs - karyopyknosis(Fig. 44, a), breaks up into lumps - karyorrhexis(Fig. 44, b) and dissolves - karyolysis. Pyknosis, rhexis and nuclear lysis are successive stages of the process and reflect the dynamics of activation of hydrolases - ribonuclease and deoxyribonuclease, which leads to the detachment of phosphate groups from nucleotides and the release of nucleic acids, which undergo depolymerization. IN cytoplasm Denaturation and coagulation of proteins occur, usually replaced by colliquation, and its ultrastructures die. Changes may affect part of the cell (focal coagulative necrosis), which is rejected, or the entire cell (coagulation of the cytoplasm). Coagulation ends plasmorexis- disintegration of the cytoplasm into clumps. On final stage destruction of the membrane structures of the cell leads to its hydration, hydrolytic melting of the cytoplasm occurs - plasmolysis. Melting in some cases covers the entire cell (cytolysis), in others - only part of it (focal liquefaction necrosis, or balloon dystrophy)(see Fig. 28, b). With focal necrosis, complete restoration of the outer cell membrane can occur. Changes in the cytoplasm (coagulation, plasmorrhexis, plasmolysis), as well as changes in the cell nucleus, are a morphological expression of the enzymatic process, which is based on the activation of hydrolytic enzymes of lysosomes.

Rice. 44. Changes in the nucleus during necrosis:

a - karyopyknosis; the nucleus (R) is reduced in size, the karyoplasm has a high electron density, the nucleolus is not differentiated; there are many vacuoles (B) in the cytoplasm, mitochondria (M) are homogenized, the Golgi complex (CG) is reduced in size; ES - endoplasmic reticulum. Electron diffraction pattern. x17,500 (according to V.G. Sharov); b - karyorrhexis. Necrosis of the splenic follicle in relapsing fever

Changes intercellular substance with necrosis, they cover both the interstitial substance and fibrous structures. Intermediate substance Due to depolymerization of its glycosaminoglycans and impregnation with blood plasma proteins, it swells and melts. Collagen fibers also swell, become impregnated with plasma proteins (fibrin), transform into dense homogeneous masses, disintegrate or lyse. Changes elastic fibers similar to those described above: swelling, basophilia, decay, melting - elastolysis Reticular fibers often persist in foci of necrosis long time, but then undergo fragmentation and clumpy decay; similar changes and nerve fibers. The breakdown of fibrous structures is associated with the activation of specific enzymes - collagenase and elastase. Thus, in the intercellular substance during necrosis, changes characteristic of fibrinoid necrosis. Less often, they manifest themselves as pronounced swelling and mucus of the tissue, which is typical liquefaction necrosis. With necrosis adipose tissue lipolytic processes predominate. Neutral fats are broken down to form fatty acids and soaps, which leads to reactive inflammation, the formation lipogranuloma(cm. Inflammation).

So, in the dynamics of necrotic changes, especially in cells, there is a change in the processes of coagulation and colliquation, but often there is a predominance of one of them, which depends both on the cause that caused the necrosis and the mechanism of its development, and on the structural features of the organ or tissue in which necrosis occurs.

With the breakdown of cells and intercellular substance in the focus of necrosis, tissue detritus. Necrosis develops around the focus demarcation inflammation.

With tissue necrosis, their consistency, color, and smell change. In some cases, dead tissue becomes dense and dry (mummification), in others - flabby and melts (myomalacia, encephalomalacia from Greek malakas- soft). Dead tissue is often pale and white-yellow in color. These are, for example, foci of necrosis in the kidneys, spleen, myocardium when blood flow is stopped, foci of necrosis due to the action of Mycobacterium tuberculosis. Sometimes, on the contrary, it is soaked in blood and has a dark red color. An example would be those arising in the background venous stagnation foci of circulatory necrosis in the lungs. Foci of necrosis of the skin, intestines, and uterus often acquire a dirty brown, gray-green or black color, as the blood pigments that permeate them undergo a number of changes. In some cases, foci of necrosis are stained with bile. When putrefactively melts, dead tissue emits a characteristic foul odor.

Classification. The cause of necrosis, the mechanism of development, and clinical and morphological features are taken into account.

Depending on the causes The following types of necrosis are distinguished: traumatic, toxic, trophoneurotic, allergic, vascular.

Traumatic necrosis is the result direct action on the tissue by physical or chemical factors. Such necrosis occurs when exposed to radiation, low (frostbite) and high (burn) temperatures, at the edges of the wound channel, and during electrical trauma. Toxic necrosis develops as a result of the action on tissue of toxins of both bacterial and non-bacterial origin, chemical compounds of different nature(acids, alkalis, medications, ethyl alcohol, etc.). Such, for example, is necrosis of the epithelium of the proximal nephron during sublimate poisoning, necrosis of cardiomyocytes when exposed to diphtheria exotoxin. Trophoneurotic necrosis occurs when there is a violation of the nervous trophism of tissues. As a result of these disorders, circulatory disorders, dystrophic and necrobiotic changes develop, ending in necrosis. These are necrosis in diseases and injuries of the central and peripheral nervous system (non-healing ulcers when damaged peripheral nerves). An example of trophoneurotic necrosis is bedsores.

Allergic necrosis tissue occurs in a sensitized organism and is, as a rule, an expression of immediate hypersensitivity reactions. Usually this fibrinoid necrosis, often found in infectious-allergic and autoimmune diseases. A classic example of allergic necrosis is the Arthus phenomenon. Vascular necrosis, which is called heart attack, occurs when blood flow in the arteries is disrupted or stopped due to thrombosis, embolism, prolonged spasm (antiogenic necrosis). Insufficient blood flow causes ischemia, hypoxia and tissue death due to the cessation of redox processes (ischemic necrosis). In the development of vascular necrosis great importance has functional tension of the organ in conditions of insufficiency of collateral circulation with narrowing of the lumen of the main arteries feeding the organ. These are, for example, ischemic necrosis of the myocardium under conditions of functional load with stenotic atherosclerosis of the coronary arteries of the heart.

Development mechanism. The mechanisms of necrosis are complex and determined by the nature of pathogenic factors, structural and functional characteristics of the tissue in which necrosis develops, the reactivity of the body, and hereditary and constitutional factors. Depending on the mechanism of action of the pathogenic factor, there are direct necrosis, caused by direct exposure (traumatic and toxic necrosis), and indirect necrosis, arising indirectly through the vascular and neuroendocrine systems (trophoneurotic, allergic, vascular necrosis).

In the prenatal period and in childhood, direct necrosis predominates, associated with the direct effect of an infectious agent or toxic substance on tissue (multiple areactive necrosis of internal organs and mucous membranes in fetuses, newborns and premature infants with generalized chickenpox, general

called smallpox vaccine, sepsis, toxoplasmosis) or due to the toxic side effects of certain medications (cytostatic agents, aminazine, etc.). Indirect necrosis, often found in adults, is observed in children as an exception with malformations of the vascular bed of a particular organ or disturbances in electrolyte metabolism.

Clinical and morphological forms of necrosis are isolated taking into account the structural and functional characteristics of the organs and tissues in which necrosis occurs, as well as the causes of its occurrence and the conditions of development. Among them there are coagulation necrosis, liquefaction necrosis, gangrene, sequestration, and infarction.

Coagulative (dry) necrosis characterized by the fact that the dead areas that arise are dry, dense, gray-yellow in color. Dry necrosis is based on the processes of protein denaturation with the formation of sparingly soluble compounds that may not undergo hydrolytic cleavage for a long time; the tissues become dehydrated. Conditions for the development of dry necrosis exist primarily in tissues rich in proteins and poor in fluids. An example would be waxy, or Zenker's(described by Zenker), muscle necrosis for infections (typhoid and typhus), trauma; cheesy necrosis for tuberculosis, syphilis, leprosy, lymphogranulomatosis; fibrinoid necrosis for allergic and autoimmune diseases.

Liquation (wet) necrosis characterized by the melting of dead tissue, the formation of cysts. It develops in tissues that are relatively poor in proteins and rich in liquid, where favorable conditions exist for hydrolytic processes. Typical wet necrosis is a focus of gray softening (ischemic infarction) of the brain. When masses of dry necrosis melt, they speak of secondary colliquation.

Gangrene(from Greek gangraina- fire) - necrosis of tissues in contact with external environment, while the tissues become gray-brown or black, which is associated with the transformation of blood pigments into iron sulfide. There are dry and wet gangrene.

At dry gangrene When exposed to air, dead tissue dries out, becomes denser, wrinkles, and becomes similar to the tissue of mummies. Therefore, dry gangrene is also called mummification(Fig. 45). Dry gangrene occurs in tissues

Rice. 45. Dry gangrene of the lower limb

poor in moisture. These are dry gangrene of the extremities with atherosclerosis and thrombosis of its artery (atherosclerotic gangrene), with frostbite or burns, fingers - with Raynaud's disease or vibration disease, skin - with infections (typhoid fever), accompanied by deep trophic disorders, etc.

At wet gangrene dead tissue is exposed to putrefactive microorganisms (Vas. perfringens, fusiformis, putrificans, histolyticus, proteus etc.), swells, becomes swollen, and emits a foul odor. Wet gangrene develops more often in tissues rich in moisture. Its occurrence is facilitated by circulatory disorders (venous stagnation) and lymph circulation (lymphostasis, edema). Wet gangrene occurs in the lungs, complicating inflammatory processes(pneumonia), in the intestines with obstruction mesenteric arteries(thrombosis, embolism). In children weakened by an infectious disease (usually measles), wet gangrene of the soft tissues of the cheeks and perineum, which is called noma (from the Greek. nome- water crayfish).

It is necessary to distinguish from dry and wet gangrene anaerobic gangrene, which is an independent infectious disease that is caused by a group of certain microorganisms (primarily You. perfringens). It occurs more often with gunshot and other wounds, accompanied by massive destruction of muscles and crushing of bones.

How is gangrene classified? bedsores - necrosis of superficial areas of the body (skin, soft fabrics) subject to pressure. Therefore, bedsores often appear in the area of ​​the sacrum, spinous processes of the vertebrae, and the greater trochanter of the femur. In its genesis, it is trophoneurotic necrosis, which usually occurs in seriously ill patients suffering from cardiovascular, oncological, infectious or nervous diseases.

Sequestration- an area of ​​dead tissue that does not undergo autolysis, is not replaced by connective tissue and is freely located among living tissues. Sequestration usually occurs in bones due to inflammation bone marrow- osteomyelitis. Around such a sequester, a sequestral capsule and a cavity filled with pus are formed. Often the sequester leaves the cavity through fistulas, which close only after its complete release. Soft tissues are also sequestered (for example, areas of lung necrosis, bedsores); such sequesters, as a rule, quickly melt.

Heart attack(from lat. infarcire- stuff, fill) - this is vascular (ischemic) necrosis, a consequence and extreme expression of ischemia. Infarction is the most common type of necrosis.

The shape, size, color and consistency of the infarction may vary. More often heart attacks occur wedge-shaped (Fig. 46-49), the base of the wedge faces the capsule, and the tip faces the gate of the organ. They are formed in the spleen, kidneys, lungs, which is determined by the nature of the angio-

Rice. 46. Splenic infarction:

a - ischemic infarction in the form of a light triangular area with its base facing the capsule; b - angioradiogram of the same spleen. Absence of vessels in the area of ​​infarction

the architectonics of these organs - the main type of branching of their arteries. Heart attacks are less common wrong shape (see Fig. 49). Such infarctions occur in the heart, brain, intestines, i.e. in those organs where it is not the main, but the scattered or mixed type of branching of the arteries that predominates. A heart attack may involve most or all of an organ (subtotal or total infarction) or can only be detected under a microscope (microinfarction). If a heart attack develops according to the type coagulative necrosis, then the tissue in the area of ​​necrosis thickens and becomes dry (myocardial infarction, kidney, spleen); if the infarction is formed according to the type of liquefaction necrosis, it softens and liquefies ( cerebral infarction, intestines).

Depending on the appearance (mainly color), three types of infarction are distinguished: white, white with hemorrhagic rim and red.

White (ischemic) infarction It is a white-yellow area, well demarcated from the surrounding tissue (Fig. 46). It usually occurs in areas with insufficient collateral circulation. It is especially common in the spleen and kidneys.

White infarction with hemorrhagic rim is represented by a white-yellow area, but this area is surrounded by a zone of hemorrhages (Fig. 47 and 49).

Rice. 47. Kidney infarction:

a - white kidney infarction with a hemorrhagic rim (sectional view); b - angioradiogram of the same kidney. Absence of vessels in the area of ​​infarction

Rice. 48. Hemorrhagic pulmonary infarction:

a - the alveoli are filled with blood; b - angioradiogram of the lung

Rice. 49. Myocardial infarction:

a - angioradiogram of the heart of a rabbit in which myocardial infarction was reproduced (ligation of the descending branch of the left coronary artery); the vessels of the ischemic zone are not injected; b - foci of ischemic infarction, surrounded by a zone of hemorrhages; c - area of ​​myocardial necrosis surrounded by granulation tissue

It is formed as a result of the fact that vascular spasm along the periphery of the infarction is replaced by their paretic expansion and the development of hemorrhages. Such an infarction is found in the kidneys and myocardium.

At red (hemorrhagic) infarction the area of ​​necrosis is soaked in blood, it is dark red and well demarcated (see Fig. 48). Favorable condition for such hemorrhagic impregnation is venous stagnation. The angioarchitecture of the organ (anastomoses between the bronchial and pulmonary arteries) is also of particular importance for the development of red infarction. Hemorrhagic infarction occurs, usually in the lungs, rarely in the intestines, spleen, and kidneys.

Greatest clinical significance have infarctions of the heart (myocardium), brain, lungs, kidneys, spleen, and intestines.

IN heart the infarction is usually white with a hemorrhagic rim, has an irregular shape, occurs more often in the left ventricle and interventricular septum (Fig. 49), extremely rarely in the right ventricle and atria. Necrosis may be localized under the endocardium (subendocardial infarction), epicardium (subepicardial infarction) or cover the entire thickness of the myocardium (transmural infarction). In the area of ​​infarction, thrombotic deposits often form on the endocardium, and fibrinous deposits on the pericardium, which is associated with the development of reactive inflammation around areas of necrosis. Most often, myocardial infarction occurs against the background of atherosclerosis and hypertension and is considered as an independent disease (see. Cardiac ischemia).

IN brain more often a white infarction occurs, which quickly softens (a focus of gray softening of the brain, Fig. 50). If a heart attack occurs against the background of significant circulatory disorders, venous stagnation, then the focus of brain necrosis becomes saturated with blood and becomes red (focus of red softening of the brain). The infarction is usually localized in the subcortical nodes, destroying the brain pathways, which is manifested by paralysis. Cerebral infarction, like myocardial infarction, most often occurs against the background of atherosclerosis and hypertension and is one of the manifestations of cerebrovascular diseases.

IN lungs in the vast majority of cases, a hemorrhagic infarction is formed (see Fig. 48). It is well demarcated, has the shape of a cone, the base of which faces the pleura. Fibrin deposits appear on the pleura in the area of ​​the infarction (reactive pleurisy). At the tip of the cone, facing the root of the lung, a thrombus or embolus is often found in a branch of the pulmonary artery. The dead tissue is dense, granular, and dark red in color.

Hemorrhagic pulmonary infarction usually occurs against the background of venous stagnation, and its development is largely determined by the characteristics of the angioarchitecture of the lungs and the presence of anastomoses between the systems of the pulmonary and bronchial arteries. In conditions of congestive plethora and closure of the lumen of the pulmonary artery branch into the area

Rice. 50. A focus of softening (right) and a cyst (left) in the brain (shown by arrows)

necrosis of lung tissue, blood enters from the bronchial artery, which breaks the capillaries and pours into the lumen of the alveoli. Inflammation of the lung tissue often develops around a heart attack. (peri-infarction pneumonia). Massive hemorrhagic infarction of the lung can cause prehepatic jaundice. White infarction in the lungs is extremely rare. It occurs with sclerosis and obliteration of the lumen of the bronchial arteries.

IN kidneys the infarction is usually white with a hemorrhagic rim; a cone-shaped area of ​​necrosis covers either the cortex or the entire thickness of the parenchyma (see Fig. 47). When the main arterial trunk is closed, it develops total or subtotal renal infarction. A unique type of heart attack is symmetrical necrosis of the renal cortex, leading to acute renal failure. The development of ischemic renal infarctions is usually associated with thromboembolism, less often with thrombosis of the branches of the renal artery, complicating rheumatism, prolonged septic endocarditis, hypertension, and coronary heart disease. Rarely, renal venous infarction occurs with renal vein thrombosis.

IN spleen white infarcts occur (see Fig. 46), often with reactive fibrinous inflammation of the capsule and subsequent formation of adhesions with the diaphragm, parietal peritoneum, and intestinal loops. Ischemic splenic infarctions are associated with thrombosis and embolism. With thrombosis of the splenic vein, sometimes venous infarctions.

IN intestines infarctions are hemorrhagic and often undergo gangrenous disintegration, which leads to perforation of the intestinal wall and the development of peritonitis.

Heart attacks are rare in the retina, liver, muscles, bones.

Reasons for development heart attack - prolonged spasm, thrombosis or artery embolism, and functional tension organ in conditions of insufficient blood supply. Of great importance for the occurrence of a heart attack is anastomotic failure And collaterals, which depends on the degree of damage to the walls of the arteries and the narrowing of their lumens (atherosclerosis, obliterating endarteritis), on the degree of circulatory disturbance (for example, venous stagnation) and on the level of shutdown of the artery by a thrombus or embolus.

Therefore, heart attacks usually occur in those diseases that are characterized by severe changes in the arteries and general circulatory disorders (rheumatic diseases, heart defects, atherosclerosis, hypertension, prolonged septic endocarditis). Acute insufficiency of collateral circulation is also caused by the development of a heart attack due to functional burden of an organ, usually the heart, the blood circulation of which is impaired. Insufficiency of anastomoses and collaterals is associated with the development venous infarctions with thrombosis

veins in conditions of congestive plethora. For the occurrence of a heart attack is also of great importance state of tissue metabolism, i.e. metabolic background against which ischemic infarction develops. Metabolism in organs and tissues in which a heart attack occurs is usually disrupted due to hypoxia caused by general circulatory disorders. Only blockage of large main arteries can lead to necrosis without previous circulatory disorders and metabolic disorders in the tissue.

Outcome of heart attack. The outcome depends on the features causative factor and the disease that complicates the heart attack, on the condition of the body and the organ in which it develops, and on the size of the heart attack.

Small foci of ischemic necrosis may be subject to autolysis followed by complete regeneration. The most common favorable outcome of a heart attack developing as dry necrosis is its organization And scar formation(Fig. 51). The organization of a heart attack may end with it petrification or hemosiderosis, if we are talking about organizing a hemorrhagic infarction. At the site of a heart attack that develops as a type of liquefaction necrosis, for example in the brain, a cyst forms.

An unfavorable outcome of a heart attack is its purulent melting, which is usually associated with thrombobacterial embolism in sepsis.

Meaning of heart attack. For the body, the significance of a heart attack is extremely great, primarily because a heart attack is ischemic necrosis. Everything that has been said about the meaning of necrosis also applies to infarction. However, it is important to note that heart attack is one of the most common and

Rice. 51. Organization of a heart attack:

a - retracted scars on the surface of the kidney after healing of the infarction; b - scar at the site of infarction in the spleen (magnifying glass)

serious complications of a number cardiovascular diseases. These are primarily atherosclerosis and hypertension. It should also be noted that heart attacks with atherosclerosis and hypertension most often develop in vital organs - the heart and brain, and this determines a high percentage of cases of sudden death and disability. The medical and social significance of myocardial infarction and its consequences made it possible to distinguish it as a manifestation of an independent disease - coronary disease hearts.

Outcome of necrosis. With a favorable outcome, reactive inflammation occurs around the dead tissue, which delimits the dead tissue. This inflammation is called demarcation, and the demarcation zone is demarcation zone. In this zone, the blood vessels dilate, plethora and edema occur, a large number of leukocytes appear, which release hydrolytic enzymes and melt (dissolve) necrotic masses. Following this, the cells multiply connective tissue, which replaces or grows over the area of ​​necrosis. When replacing dead masses with connective tissue, they speak of them organizations. In such cases, at the site of necrosis, a scar(scar at the site of the infarction - see Fig. 51). Fouling of the necrosis area leads to its encapsulation(Fig. 52). Calcium salts can be deposited in the dead masses during dry necrosis and in the focus of necrosis that has undergone organization. In this case, it develops calcification (petrification) focus of necrosis (see. Mineral dystrophies). In some cases, bone formation is noted in the area of ​​necrosis - ossification. When tissue detritus is absorbed and a capsule is formed, which usually occurs with wet necrosis and most often in the brain, a cavity appears at the site of necrosis - a cyst (see Fig. 50).

Unfavorable outcome of necrosis - purulent melting of the necrosis focus. This is the purulent melting of heart attacks during sepsis (such heart attacks are called septic). As a result of necrosis in the early stages of intrauterine development, a defect of an organ or part of the body occurs.

The meaning of necrosis. It is determined by its essence - “local death”, therefore necrosis is vital important organs often leads to death. These are myocardial infarctions, ischemic necrosis of the brain, necrosis of the cortical

Rice. 52. Area of ​​necrosis (bottom) surrounded by a fibrous capsule (encapsulation of necrosis)

kidney substances, progressive liver necrosis, acute pancreatic necrosis. Often tissue necrosis is the cause severe complications many diseases (heart rupture with myomalacia, paralysis with hypertensive stroke, infections with massive bedsores, etc.), as well as intoxication due to the impact of tissue decay products on the body (for example, with gangrene of the limb). Purulent melting of the necrosis focus may be the cause purulent inflammation serous membranes, bleeding, sepsis. With the so-called favorable outcome of necrosis, its consequences are very significant if it occurred in vital organs (cyst in the brain, scar in the myocardium).

Death, signs of death, postmortem changes

Death How biological concept is an expression of the irreversible cessation of the body’s vital functions. With the onset of death, a person turns into a dead body, a corpse (cadaver).

Depending on the causes, leading to death, a distinction is made between natural (physiological), violent and death from disease.

Natural death occurs in people old age and long-livers as a result of natural (physiological) wear and tear of the body (physiological death). The lifespan of a person has not been established, however, if we are guided by the life expectancy of the centenarians of our planet, it can be 150 years or more.

The interest in the problem of old age and aging, which is dealt with by a special branch of medical and biological science, is understandable - gerontology (from Greek geron- old and logos- teaching), and to diseases of old age studied geriatrics (from Greek geron- old and iatreia- treatment), which is a branch of gerontology.

Violent death observed as a result of such actions (intentional or unintentional) as murder, suicide, death from various types of injuries (for example, street, industrial or domestic injury), accidents (for example, a transport accident). Violent death, being a socio-legal category, is studied by forensic medicine and justice authorities.

Death from disease arises as a result of the incompatibility of life with those changes in the body that are caused by pathological (painful) processes. Typically, death from the disease occurs slowly and is accompanied by a gradual decline in vital functions. But sometimes death occurs unexpectedly, as if in the midst of complete health - sudden, or sudden death. It is observed in cases of latent or sufficiently compensated disease, in which a fatal complication suddenly develops (excessive bleeding due to rupture of an aortic aneurysm, acute myocardial ischemia due to thrombosis of the coronary artery of the heart, cerebral hemorrhage due to hypertension, etc.).

Depending on the development of reversible or irreversible changes

vital functions of the body distinguish between clinical and biological death.

Clinical death characterized by cessation of breathing and blood circulation, however, these changes in the vital activity of the body are reversible within a few minutes (the time it takes to experience the cerebral cortex). At the core clinical death lies a peculiar hypoxic state (primarily the central nervous system) due to the cessation of blood circulation and the absence of its central regulation.

The onset of clinical death is preceded by agony(from Greek agon- struggle), reflecting the uncoordinated activity of homeostatic systems in the terminal period (arrhythmias, sphincter paralysis, convulsions, pulmonary edema). Therefore, agony, which can last from several minutes to several hours, is referred to as the so-called terminal conditions, ending in clinical death. At terminal states(agony, shock, blood loss, etc.) and clinical death, a resuscitation complex is used (from Lat. re And animation- revitalization) of events. The basic patterns of extinction and restoration of human vital functions are studied by a special branch of medicine called resuscitation.

Biological death- irreversible changes in the functioning of the body, the beginning of autolytic processes. However, the death of cells and tissues upon the onset of biological death does not occur simultaneously. The first to die is the central nervous system; already 5-6 minutes after breathing and circulation stop, the ultrastructural elements of the parenchymal cells of the brain and spinal cord are destroyed. In other organs and tissues (skin, kidneys, heart, lungs, etc.) this process lasts for several hours and even days; the general structure of many organs and tissues, observed after death under a light microscope, is preserved for quite a long time, only with electronic -microscopic examination reveals destruction of cell ultrastructures. Therefore, a pathologist, studying microscopically material taken from a corpse, can judge the nature of pathological changes in organs and tissues.

Due to the fact that after death the death of many organs and tissues extends over a relatively for a long time, material taken from a corpse is used for transplantation (transplantation) of organs and tissues. Currently, cadaveric blood for transfusion, preserved tissue (cornea, skin, bones, blood vessels) and cadaveric organs (kidney) for transplantation are widely used in clinical practice.

Soon after the onset of biological death, a number of signs of death And posthumous changes: cooling the corpse; rigor mortis; cadaverous desiccation; blood redistribution; cadaveric spots; cadaveric decomposition.

Cooling a corpse (algor mortis) develops due to the cessation of heat production in the body after death and the equalization of temperature

dead body and environment. If before death the patient had a very high temperature or convulsions were observed during a long atonal period, then the cooling of the corpse occurs slowly. In some cases (death from tetanus, strychnine poisoning), the temperature of the corpse may rise in the immediate hours after death.

Rigor mortis (rigor mortis) is expressed in the compaction of voluntary and involuntary muscles. It is caused by the disappearance of adenosine triphosphoric acid from the muscles after death and the accumulation of lactic acid in them. Rigor mortis usually develops 2-5 hours after death and by the end of the day covers all the muscles. First, the masticatory and facial muscles undergo rigor, then the muscles of the neck, torso and limbs. The muscles become dense: in order to bend a limb at a joint, significant force has to be applied. Rigor mortis persists for 2-3 days, and then disappears (resolves) in the same sequence in which it appears. If rigor mortis is forcibly destroyed, it does not appear again.

Rigor mortis is severe and develops quickly in individuals with well-developed muscles, as well as in cases where death occurs due to convulsions (for example, tetanus, strychnine poisoning). Rigor mortis is mildly expressed in the elderly and children, in people who are exhausted and have died from sepsis; In premature fetuses, rigor mortis is absent. Low temperature environment makes the onset of rigor mortis difficult and lengthens the period of its existence, high temperature accelerates the resolution of rigor mortis.

Corpse desiccation occurs due to the evaporation of moisture from the surface of the body. It may be limited to individual areas, but the entire corpse may dry out. (mummification of a corpse). First of all, drying affects the skin, eyeballs, mucous membranes. Associated with drying clouding of the corneas, the appearance on the sclera when the palpebral fissure is open, dry brownish triangular spots; the base of these spots faces the cornea, and the top faces the corner of the eye. The mucous membranes become dry, dense, and brownish in color. On the skin, dry, yellow-brown, parchment-like spots appear primarily in places of maceration or damage to the epidermis. So-called parchment spots from drying out can be mistaken for intravital abrasions and burns.

Blood redistribution in a corpse it is expressed in the veins being overflowing with blood, while the arteries are almost empty. Post-mortem blood coagulation occurs in the veins and cavities of the right half of the heart. The resulting post-mortem blood clots have a yellow or red color, a smooth surface, elastic consistency (stretch) and lie freely in the lumen or chamber of the heart, which distinguishes them from blood clots. When death occurs quickly, there are few post-mortem clots; when death occurs slowly, there are many.

When dying in a state of asphyxia (for example, asphyxia of newborns), the blood in the corpse does not clot. Over time, cadaveric hemolysis occurs.

Cadaveric spots arise in connection with the redistribution of blood in the corpse and depend on its position. Due to the fact that blood flows into the veins of the underlying parts of the body and accumulates there, 3-6 hours after death, the formation of cadaveric hypostases. They look like dark purple spots and turn pale when pressed. Corpse hypostases are absent in areas of the body exposed to pressure (the area of ​​the sacrum, shoulder blades when the corpse is positioned on the back). They are well expressed in cases of death from diseases leading to general venous stagnation, and poorly in cases of anemia and exhaustion.

Subsequently, when postmortem hemolysis of red blood cells occurs, the area of ​​cadaveric hypostases is saturated with blood plasma diffusing from the vessels and stained with hemoglobin. Late cadaveric spots appear, or corpse imbibition. These spots are red-pink in color and do not disappear with pressure.

Corpse decomposition associated with the processes of autolysis and decay of the corpse. Post-mortem autolysis occurs earlier and is more intensely expressed in glandular organs (liver, pancreas, stomach), the cells of which are rich in hydrolytic (proteolytic) enzymes. Postmortem self-digestion of the pancreas occurs very early. Due to the activity of gastric juice, post-mortem self-digestion of the stomach occurs (gastromalacia). When gastric contents are thrown into the esophagus, self-digestion of its wall (esophagomalacia) is possible, and when gastric contents are aspirated into the respiratory tract, “acidic” softening of the lungs occurs. (pneumomalacia acida).

Post-mortem autolysis is quickly joined putrefactive processes due to the proliferation of putrefactive bacteria in the intestines and their subsequent colonization of the tissues of the corpse.

Rotting intensifies post-mortem autolysis, leading to the melting of tissues, which turn dirty green (iron sulfide is formed from the action of hydrogen sulfide on the breakdown products of hemoglobin) and emit a foul odor.

Gases formed during the rotting of a corpse swell the intestines, penetrate into the tissues and organs, which acquire a foamy appearance, and crepitus is heard when palpated ( cadaveric emphysema). The rate of cadaveric autolysis and putrefaction depends on the ambient temperature. In this regard, corpses are stored in refrigerators. Suspends cadaveric decomposition and embalming, which can be used to preserve corpses for a long time. However, embalming changes the appearance of organs and makes it difficult to assess the nature of their changes during pathological or forensic examination.

Necrosis is one of the variants of local death, which can involve cells, groups of cells, tissues, organs and occurs in the presence of strong damaging factors.

Etiological types of necrosis:

1. Traumatic = occurs under the action of physical (mechanical, temperature, radiation, etc.) and chemical (acids, alkalis, etc.) factors.

2. Toxic = occurs under the action of toxins of bacterial and other nature.

3. Trophoneurotic - associated with impaired microcirculation and tissue innervation in chronic diseases.

4. Allergic - develops as a result of immunopathological reactions.

5. Vascular = associated with impaired blood supply to an organ or tissue.

Depending on the mechanism of action of the etiological factor, the following are distinguished:

A. Direct necrosis (with direct action on tissue due to traumatic and toxic damage).

6. Indirect (mediated action through the vascular, nervous and immune systems).

Morphogenesis of necrosis. The following stages of development of necrosis are distinguished.

I. Paranecrosis = necrotic-like reversible changes.

II. Necrobiosis is irreversible degenerative changes.

III. Cell death (there are currently no criteria for establishing the moment of cell death).

IV. Autolysis = decomposition of dead substrate by hydrolytic enzymes released from the damaged cell.

The decomposition of a cell under the action of enzymes released from incoming leukocytes or under the influence of bacteria is called “heterolysis”.

Depending on the predominance of protein denaturation in dead structures or enzymatic digestion, two main types of necrosis occur: coagulation and colliquation.

Morphology. Morphological signs of necrosis (macro- and microscopic) appear only at the stage of autolysis, i.e. several hours after cell death occurs.

In the heart, for example, the first morphological signs of necrosis are usually detected only after 12 - 18 hours from the moment of ischemia (in the heart, ischemic, i.e., vascular, necrosis - infarction more often occurs), but the disappearance of enzymes (succinate dehydrogenase, lactate dehydrogenase, etc.) glycogen from a necrotic cell, the breakdown of ultrastructures can be detected much earlier.

Early signs of necrosis are detected using electron microscopic and histochemical studies.

A. Electron microscopic picture: in the zone of myocardial ischemia, swelling and vacuolization of mitochondria and disintegration of cristae are detected.

B. Histochemical examination (with the PHIK reaction) reveals the disappearance of glycogen from the ischemic zone, while in the remaining areas it turns crimson.

Macroscopic signs can manifest themselves in different ways: they depend on the specificity of the organ in which necrosis occurs, as well as on the nature of the damaging factor.

Microscopic signs concern both the nucleus and cytoplasm of cells, as well as the extracellular matrix.

A. Kernel changes:

° karyopyknosis - shrinkage of nuclei due to chromatin condensation;

° karyorrhexis - disintegration of nuclei into clumps;

° karyolysis - dissolution of the nucleus due to the activation of hydrolases (ribonuclease and deoxyribonuclease).

B. Changes in the cytoplasm:

° plasma coagulation denaturation and coagulation of protein with the appearance of bright pink lumps in the cytoplasm;

° plasmorhexis - disintegration into clumps;

° plasmolysis - melting of the cytoplasm.

B. Changes in the extracellular matrix are manifested in the splitting of reticular, collagen and elastic fibers under the influence of proteases and lipases. Necrotic masses are often impregnated with fibrin with the development of fibrinoid necrosis.

Reaction to necrosis of surrounding tissues. Demarcation inflammation occurs around the area of ​​necrosis. Its feasibility lies in delimiting the focus of necrosis, participating in the resorption of necrotic masses with subsequent organization, i.e. replacing them with connective tissue.

Clinical and morphological forms of necrosis are represented by coagulation, liquefaction necrosis, infarction, sequestration and gangrene.

1. Coagulation (dry) necrosis is characterized by the predominance of coagulation, dehydration, and compaction processes in dead tissues.

Necrotic tissues are dry, dense, gray-yellow in color.

Examples of coagulative necrosis include cheesy, fibrinoid and waxy necrosis; A special type is adipose tissue necrosis - fat necrosis.

Cheesy (caseous) necrosis:

° areas of necrosis are dry, whitish, crumbling;

° develops with tuberculosis, syphilis.

B. Fibrinoid necrosis:

° found in interstitial tissue and vascular walls, necrotic masses are impregnated with plasma proteins and fibrinogen;

° occurs in immunopathological processes, allergic diseases.

B. Waxy (Zenker's) necrosis:

° occurs in skeletal muscles, most often the rectus and oblique abdominal muscles and the adductor muscle of the thigh;

° develops in acute infectious diseases (typhoid, typhus) and trauma.

G. Fat necrosis:

° comes in two forms:

1) traumatic fat necrosis(in case of damage to fatty tissue);

2) enzymatic fat necrosis occurs in acute pancreatitis: enzymes from damaged gland cells cause lipolysis, the resulting fatty acids form calcium salts (soaps).

2. Liquation (wet) necrosis is characterized by the melting of necrotic tissue and its hydration.

Found in tissues with high water content.

An example is gray softening (ischemic infarction) of the brain, in which a focus of flabby consistency is detected irregular shape gray color.

As a rule, wet necrosis results in the formation of a cyst.

3. Heart attack - tissue necrosis that occurs when blood circulation is impaired (vascular, ischemic necrosis).

Develops as a result of thrombosis, embolism, prolonged arterial spasm or functional overstrain of an organ in conditions of insufficient blood supply (the latter applies only to myocardial infarction). The shape of the infarction is determined by the angioarchitecture and can be wedge-shaped or irregular:

A) wedge-shaped infarction is typical for organs with a main type of vessel branching and with underdeveloped collaterals (spleen, kidney, lung);

B) an irregular form of infarction is observed in organs with a scattered type of blood supply and an abundance of anastomoses (myocardium, brain).

In appearance, the infarction can be white (ischemic), red (hemorrhagic) and white with a hemorrhagic rim.

The shape and type of infarction depend on the uniqueness of the organ’s vascular system (type of branching of vessels, the presence and level of development of anastomoses and other features of the blood supply) and its structural and functional features.

1) Ischemic (white) infarction usually occurs in areas of insufficient collateral blood supply, which excludes the flow of blood into the area of ​​necrosis.

Most often occurs in the brain and spleen.

A. Ischemic cerebral infarction:

° occurs more often with atherosclerosis and hypertension;

° immediate causes of development

Thrombosis,

Thromboembolism;

° macroscopically: a focus of irregular shape, a flabby consistency of a grayish color (a focus of gray softening).

B. Ischemic infarction of the spleen:

° the most common reason- thromboembolism;

° macroscopic signs: the lesion is triangular in shape, white, dryish, of dense consistency, with its base facing the capsule and bulging under the capsule; the capsule in the area of ​​the infarction is rough and covered with fibrinous deposits.

2) White infarction with a hemorrhagic rim occurs when vascular spasm along the periphery of the infarction is replaced by paretic expansion and the development of diapedetic hemorrhages.

Often occurs in the myocardium and kidneys.

A. Myocardial infarction:

°macroscopic picture: in the wall of the left ventricle or interventricular septum a focus of irregular shape, flabby consistency, yellowish-white color, surrounded by a hemorrhagic rim is determined;

°microscopic picture: in the zone of necrosis, cardiomyocytes devoid of nuclei (karyolysis) are visible, with clumpy disintegration of the cytoplasm (plasmorhexis); along the periphery of necrosis, demarcation inflammation is noted in the form of vascular congestion and tissue infiltration with polymorphonuclear leukocytes; in the remaining areas of the myocardium - dystrophic changes in cardiomyocytes.

B. Kidney infarction:

°macroscopic picture: a triangular-shaped area, with its base facing the capsule, surrounded by a dark red corolla;

° microscopic picture: in the zone of necrosis, only the contours of the glomeruli and tubules are preserved, their cells lack nuclei (karyolysis), in some places the cytoplasm is lysed in these areas, structureless pink masses are visible (necrotic detritus); along the periphery - a zone of demarcation inflammation, in which full-blooded vessels, hemorrhages, and accumulations of polymorphonuclear leukocytes are visible; then the surviving kidney tissue, in the tubular epithelium - dystrophic changes.

3) Hemorrhagic (red) infarction usually occurs under conditions of venous stagnation, and the angioarchitecture of the organ is of great importance.

Most often occurs in the lungs with thromboembolism or thrombosis of the branches of the pulmonary artery in conditions of venous congestion.

Mechanism: in conditions of congestive plethora and closure of a branch of the pulmonary artery (thrombosis, thromboembolus), blood from the bronchial artery rushes through the anastomoses under high pressure into the area of ​​necrosis, and the capillaries rupture and the necrotic tissue is impregnated with red blood cells.

Macroscopic picture: pulmonary infarction is triangular in shape, dark red in color, dense in consistency, with its base facing the pleura, with fibrinous deposits on the pleura in this area.

Microscopic picture: in the area of ​​necrosis, a rupture of the interalveolar septa, the absence of nuclei in the septal cells and alveolar epithelium are determined; the area of ​​necrosis is saturated with blood; in the zone of demarcation inflammation there are accumulations of leukocytes; the remaining lung tissue is highly airy (emphysema).

There are 2 stages of infarction: necrotic and organizational. During the organization stage, young connective (granulation) tissue appears in the zone of demarcation inflammation, which gradually replaces necrosis and, when maturing, leads to the formation of a scar at the site of the infarction.

4. Sequestration is an area of ​​dead tissue that does not undergo autolysis, is not replaced by connective tissue and is freely located among living tissues.

As a rule, it is accompanied by the development of purulent inflammation with the formation of fistulous tracts through which fragments of the sequester can escape. Occurs predominantly in bones.

5. Gangrene = necrosis of tissues in contact with the external environment and having a black color as a result of the formation of iron sulfide.

There are three morphological varieties gangrene: dry, wet and bedsores.

A. Dry gangrene is accompanied by mummification, a well-defined zone of demarcation inflammation.

Often occurs in the lower extremities.

Macroscopic picture: necrotic tissue (usually the feet) is reduced in volume, dry, black, with a well-defined demarcation zone.

6. Wet gangrene develops in tissues with the addition of putrefactive flora.

The tissue swells, becomes edematous, and the demarcation zone is not defined.

Occurs in the intestines, lungs, uterus, and limbs.

Gangrene of the intestines.

Macroscopic picture: the intestinal loop is thickened, edematous, flabby consistency, black-red in color, the serous membrane is dull, covered with fibrin.

B. Bedsore. A type of gangrene that occurs as a result of trophoneurotic disorders in weakened bedridden patients in areas of the body exposed to the greatest pressure.

Favorable outcomes of necrosis are associated with the processes of demarcation and repair spreading from the zone of demarcation inflammation:

° organization, or scarring - replacement of necrotic masses with connective tissue;

° encapsulation = delimitation of the area of ​​necrosis by a connective tissue capsule;

° petrification - impregnation of the necrosis area with calcium salts (dystrophic calcification);

° ossification = the appearance of bone tissue necrosis in the area (very rare, in particular, in Gohn's lesions - healed foci of primary tuberculosis);

° cyst formation as a result of liquefaction necrosis.

The outcome is unfavorable - purulent melting of necrotic masses, with the possible development of sepsis.

Even in the modern world, anyone can face such a problem as tissue necrosis. In this article, this disease will be discussed.

What it is

First of all, you need to understand the concepts themselves that will be actively used in this article.

Necrosis is a process that does not have a reverse nature. With this disease, tissue cells or parts of organs gradually die. One can even say that this is the end result of the breakdown of tissues of a still living and functioning organism. Important: necrosis is also called gangrene (this is one of the subtypes of the disease). This disease develops exclusively in those tissues that have the prerequisites for death, i.e. in previously damaged ones.

Causes

It is also necessary to talk about why tissue necrosis can occur in a living organism. What are the prerequisites for the occurrence of this terrible disease? So, generally speaking, gangrene begins to develop in those organs or tissues where blood circulation is impaired. And the further the body part is from the main blood vessels, the more likely he is to become infected.

1. Physical reasons. This can be the influence of low or high temperature, gunshot wound, electric shock and even radiation.
2. Biological. Protozoa organisms can cause tissue necrosis: viruses, bacteria.
3. Allergic. For example, with infectious and allergic diseases, fibroid necrosis may occur in some tissues.
4. Vascular. A heart attack is the same as vascular necrosis. It is associated with impaired blood circulation in organs or tissues.
5. Toxic causes. Various chemicals and toxins that damage body tissue can cause gangrene.
6. Trophoneurotic. In this case, tissue death is caused by non-healing ulcers and bedsores. The disease is associated with tissue innervation, as well as with impaired blood microcirculation.

Tissue necrosis can occur due to certain diseases. So, diabetes mellitus may be the cause of this disease. Damage to the spinal cord or large nerves can also contribute to the occurrence of necrosis.

About the types of disease

I would definitely like to say that tissue necrosis can be classified. What could this disease be, depending on the mechanism of action?

1. Direct necrosis. It occurs as a result of injuries, poisoning by toxins, or due to the work of certain microorganisms.
2. Indirect necrosis. It occurs indirectly, through body systems such as the cardiovascular or neuroendocrine. These can be allergic, trophoneurotic and vascular necrosis.

IN medical practice There are two more types of this disease:

1. Liquation necrosis. Along with tissue necrosis, tissue swelling occurs.
2. Coagulative necrosis. With this subtype of the disease, along with tissue necrosis, complete dehydration occurs.

Symptoms

Is it possible to independently recognize tissue necrosis? Symptoms of this disease may be as follows:

1. Lack of sensitivity, numbness of the tissue.
2. Pallor skin(this may be the so-called “waxy” skin).
3. If you do not deal with the previous symptom, the skin first begins to turn blue, then turn green or black.
4. If the disease affects the lower limbs, it becomes difficult for the patient to walk. Feet can also get cold even at high temperatures.
5. Lameness in the legs and muscle twitching may occur.
6. Also, ulcers often begin to appear that do not heal. It is with this symptom that gangrene begins.

Stages of the disease

A very terrible disease in its nature and end result is tissue necrosis (photos of patients with such a disease are the first confirmation). However, it is worth saying that this disease occurs in several stages.

1. Paranecrosis. These changes are still reversible; if treated in time, the disease can be eliminated without any negative consequences for the body.
2. Necrobiosis. These changes are already irreversible. In this case, important tissue metabolism is disrupted, which prevents the formation of new healthy cells.
3. Cell death.
4. Autolysis. This is already a process of complete tissue decomposition. It occurs under the action of enzymes that release dead cells.

Coagulative necrosis

It most often affects those parts human body, which are rich in proteins, but also poor in various body fluids. For example, this may be coagulative necrosis of liver cells (adrenal glands or spleen), where lack of oxygen and poor blood circulation most often occur.

Subtypes of coagulative necrosis

There are several subtypes of so-called “dry” necrosis:

1. Heart attack. This is vascular tissue necrosis. By the way, the most common disease.
2. Curdled or caseous necrosis. Occurs if a person has diseases such as leprosy, syphilis, tuberculosis. With this disease, a piece of dead tissue is found on the internal organs, it can crumble. If the patient is syphilitic, areas of dead tissue will appear as a whitish liquid (similar to cottage cheese).
3. Zenker's, or waxy, necrosis. This subtype of the disease affects muscle tissue.
4. Fibrinoid necrosis. This is the death of areas of connective tissue. The causes of its occurrence are most often autoimmune or allergic diseases.
5. Fat necrosis. It, in turn, is divided into enzymatic (most often occurs in diseases of the pancreas) and non-enzymatic fat necrosis (this is necrosis of adipose tissue that accumulates under the skin and is also found in the mammary glands).
6. Gangrene.

A few words about gangrene

I would definitely like to say a few words about such a disease as gangrene. This is one of the subtypes of tissue necrosis. It affects areas of the body that are actively in contact with the external environment. Why was this disease identified in separate group? It’s simple; often when the skin is affected by gangrene, it also becomes infected with bacteria. And along with this, the disease undergoes secondary changes. Scientists distinguish the following types of gangrene:

1. Dry. In this case, tissue necrosis occurs without the participation pathogens. Occurs most often on the patient’s extremities. This may be atherosclerotic gangrene (occurs as a result of a disease such as vascular atherosclerosis); gangrene, which occurred due to exposure to temperatures (burn or frostbite of the skin); gangrene that affects the fingers (vibration disease or Raynaud's disease), or gangrene that affects the skin during infectious rashes (for example, during typhus).
2. Wet gangrene. It occurs as a result of the attachment of a bacterial infection to dead tissue. It develops most often in internal organs. Infection often results in bad smell. This type of gangrene can be fatal.
3. Gas gangrene. Occurs after infection of the wound with anaerobic flora. As a result of the disease, a large area of ​​tissue becomes infected and gas is formed. The main symptom: crackling under the fingers during palpation. It is worth saying that the percentage of deaths is also quite high.
4. Bedsores. This is the necrosis of individual areas of tissue under pressure. They occur most often in bedridden patients. In this case, the nerves and blood vessels are compressed, blood circulation is disrupted, and this disease occurs.

Aseptic necrosis

Aseptic necrosis develops due to disruption of the blood flow of the vessels that supply the head of the femur (this is the so-called “hinge” of the femur). It is worth saying that this disease affects men seven times more often than women. The age of the disease is young. It most often occurs in people between 20 and 45 years old. An important point: avascular necrosis is very similar to arthrosis of the hip joint in its symptoms. Therefore, these diseases are very often confused. However, the course of these diseases is different. If arthrosis develops slowly, then necrosis affects a person rapidly. Main symptoms:

• Pain in the groin.
• Pain when walking.
• Appearance of lameness.
• Restricted mobility of the affected leg.
• Atrophy of the thigh muscles.
• There may be either shortening or lengthening of the leg affected by necrosis.

As for treatment, its success depends entirely on the extent of the disease. How can you diagnose bone necrosis in the early stages of the disease:

1. Computed tomography - CT.
2. Magnetic resonance imaging - MRI.

It is impossible to detect bone necrosis at an early stage using x-rays. On x-ray you can already see signs aseptic necrosis. It is also impossible to identify this disease using tests. As for treatment, in this case it will be aimed at improving blood circulation in the artery of the femoral head. Anti-inflammatory drugs and analgesics will also be effective. Surgical intervention for this type of disease is most often not required.

Necrosis and pregnancy

Sometimes pregnant women are diagnosed with decidual tissue with necrosis. What does this mean? So, first of all, I would like to say that the decidual tissue itself plays important role at the moment of implantation of the fertilized egg. It eliminates various damage to the walls of the uterus. And if it begins to die, this is a signal that the unborn child needs the care of qualified specialists. As a result of infection of this tissue, blood circulation will be impaired, which can cause not only the breakdown of decidual tissue, but also fetal rejection.

Consequences of necrosis

Regardless of the cause of this disease in the patient (it will be tissue necrosis after an injection or infectious necrosis), the consequences of the disease can be very different (if timely competent treatment). So, what could be the consequences of necrosis:

1. Scarring or replacement. In this case, the necrotic masses are replaced by connective tissue.
2. Removal of dead cells. This occurs thanks to phagocytes and lysosomal enzymes of leukocytes.
3. Encapsulation. In this case, the focus of necrosis is limited to the connective tissue.
4. Cell calcification. In this case, areas of dead tissue are saturated with calcium salts.
5. Ossification. Here, bone tissue begins to form in the dead areas.
6. Cyst formation.
7. Melting of tissue with pus. Sepsis is often the consequence. This is an unfavorable outcome of necrosis, when areas of dead tissue do not undergo autolysis.

Treatment

If the patient has tissue necrosis, treatment will depend on multiple factors. So, the causes of the disease, the type of disease, as well as the degree of tissue damage will be important. At the very beginning, I would like to say that the earlier necrosis is detected, the easier it will be for the patient to cope with the problem. The danger of the disease is that it can be fatal. That is why, when the very first symptoms or even doubts about tissue death appear, you should seek medical help. Self-medicating in this case can be a life-threatening activity.

Bedsores

If a patient has bedsores, the patient needs high-quality daily care. In this case it is necessary:

1. Ensure that the patient's bed is clean, level, and moderately hard. There should be no folds on the sheet.
2. The patient should be turned as often as possible.
3. It is also important to rub bedsores and massage the lesions as often as possible. Do everything to improve blood circulation in these affected areas.
4. Bedsores should also be lubricated with salicylic or camphor alcohol.
5. Inflatable rings specially designed for such cases should be placed under the patient’s lower back or sacrum.

Dry necrosis

If the patient has so-called dry tissue necrosis, treatment will be carried out in two stages:

1. Drying tissues, as well as preventing the subsequent development of infection.

• The skin around the area affected by necrosis will be treated with an antiseptic.
• Next, a bandage soaked in ethyl alcohol or drugs such as Boric acid and Chlorhexedine.
• It is also very important to dry the area affected by necrosis. This is done using potassium permanganate (5% solution of potassium permanganate) or brilliant green.

1. The next stage is the excision of non-viable tissue. There may be cutting off the foot, resection of the phalanx (it all depends on the degree of necrosis).

A small conclusion: if the patient has necrosis, treatment will be aimed primarily at restoring blood circulation in the affected areas. It will also be necessary to exclude the cause of tissue damage due to necrosis. And, of course, the patient will be prescribed antibacterial therapy. This is necessary in order to avoid infection of dead tissue bacterial infection(after all, this is precisely what can lead to death).

Wet necrosis

If the patient has wet necrosis of the skin or other tissue, then treatment will depend on the degree of damage to the patient. At the very beginning, doctors will try to convert wet necrosis into the category of dry necrosis (however, this is only possible in the early stages of the disease). If this fails, you will have to resort to surgery.

Local treatment for wet necrosis

What will doctors do in this case:

1. It is necessary to regularly wash the wound with a solution of hydrogen peroxide (3%).
2. The so-called pockets and leaks will be opened, it is necessary various ways drainage.
3. It is also important to apply antiseptic dressings. To do this, you can use drugs such as Furacilin, Chlorhexedine, Boric acid.
4. It will also be mandatory therapeutic immobilization(applying plaster splints).

General treatment for wet necrosis

If the patient has wet tissue necrosis (after surgery or for other reasons), then general treatment measures will be necessary.

1. Antibacterial therapy. In this case, the patient will be given antibiotics intravenously or intra-arterially.
2. Vascular therapy. Doctors will try to restore blood circulation in the tissues affected by necrosis.
3. Detoxification therapy. The efforts of specialists will be aimed at preventing infection of living tissues that are located near the site of necrosis.

Surgical intervention

If a patient, for example, has wet necrosis of soft tissues, treatment may no longer help him. In this case you will need surgery. Those. Surgeons should begin working with the patient. As mentioned above, at the very beginning of treatment, specialists will try to convert wet necrosis into dry, this can take no more than a couple of days. If no positive results are observed, the patient will have to be sent for surgery. By the way, in this case this is the only way to save the patient’s life.

1. Preoperative preparation. This will require antibacterial and infusion therapy.
2. Operation. Removal of necrosis within still intact and viable tissue. However, doctors know that pathogenic bacteria may already be in healthy tissues. Therefore, the so-called “high” amputation is most often welcomed, when part of the healthy tissue is excised along with the affected area.
3. Postoperative period. If necrosis of the patient’s skin ends with surgery and removal of part of the limbs, then not only medical support for the patient will be required for some time after the operation, but also psychological support.

Folk remedies

As mentioned above, a disease such as tissue necrosis is quite scary and dangerous (photos of patients affected by this disease are another confirmation of this). In this case, it is best to resort to medical care, since only qualified specialists can help solve the problem. However, in this case, traditional medicine often becomes useful. But it is best to be treated in this way only with the doctor’s permission or in extreme situations when it is impossible to obtain qualified doctor’s help.

1. If a patient has a problem such as bedsores, they can be dealt with in the following ways. So, you need to lubricate the affected areas with sea buckthorn oil. You can make lotions from rosehip oil (all this is sold at the pharmacy).
2. Ointment for bedsores. To prepare it, you need to take crushed oak bark (two parts), black poplar buds (1 part) and butter(6-7 parts). The ingredients are mixed, infused overnight in a warm place, after which everything is boiled and filtered. After this, the ointment is ready for use.
3. Ointment for necrosis. To prepare it, you need to mix a tablespoon of lard with one teaspoon of slaked lime and the same amount of ash obtained after burning oak bark. This mixture is applied to the wound, tied with a bandage, and left overnight. In the morning everything needs to be removed. You need to do this three evenings in a row.
4. Treatment of soft tissue skin necrosis can be carried out using a herbal decoction. To prepare it, you need to pour two kilograms of ordinary chestnut fruit with water so that the ingredients are completely covered. Everything is boiled for about 15 minutes. After this, the water is poured into a jar, and the chestnuts are filled with fresh water. The procedure is repeated again. After this, the resulting liquids are mixed and simmered over low heat until two liters of liquid remain. Next you need to take half a liter of broth, add 5 liters cold water and make baths. The procedures must be repeated daily until the problem disappears.

Irreversible processes of necrosis of body tissue under the influence of internal or external agents are called necrosis in medicine. For a person, this pathological condition is very dangerous and can lead to serious consequences. Treatment of necrotic changes should be carried out strictly under the supervision of highly qualified doctors in a hospital setting.

Causes of tissue necrosis

Before treating a dangerous disease, it is important to find out what factors provoke it. Mostly tissue death begins due to circulatory problems. In some cases, necrosis develops due to diabetes mellitus, damage to large nerves, spinal cord injuries. Other possible causes of tissue breakdown are described below:

1. Physical necrosis develops under the influence of low or high temperatures, radiation, electric current, various injuries, gunshot wounds And so on.
2. Biological tissue necrosis occurs under the influence of bacteria and viruses.
3. Allergic necrosis develops due to infection infectious diseases, provoked by a certain irritant, causing fibrinoid tissue lesions.
4. Toxic necrosis appears under the influence of toxic substances on the patient’s body.
5. Vascular necrosis (infarction) develops when blood circulation in human tissues and internal organs is impaired.
6. Trophic death causes bedsores and non-healing wounds. The condition develops after a disruption in the process of blood microcirculation or innervation (connection of organs with the central nervous system).

Types of tissue necrosis

To assess the nature of the pathology and prescribe the correct treatment, it is necessary to determine the type of necrotic damage. The disease is classified according to clinical, etiological and morphological characteristics. Belonging to a particular group depends on the conditions for the development of the pathology and the characteristics of the affected tissue. The following types of necrosis are distinguished:

1. Dry (coagulative) affects structures saturated with protein (spleen, kidneys, liver). It is characterized by dehydration and compaction. This type includes caseous (curd-like), Zenker's (waxy), fibrinoid lesions, necrosis of adipose tissue.
2. Wet (colliquation) affects structures rich in moisture (spinal cord or brain). The disease develops due to autolytic breakdown, causing liquefaction.
3. A heart attack develops due to a sudden complete or partial disruption of the blood supply to organs.
4. Bedsores are local lesions due to poor circulation caused by constant compression.
5. Gangrene develops when tissue comes into contact with the external environment. Depending on the location, it is divided into gas, dry, and wet. Characterized by edema and crepitus, depending on the specific type.
6. Sequestrum is an area of ​​dead structure (mainly bone) that does not undergo autolysis (self-dissolution).

Origin pathological condition matters too. Based on this parameter, tissue death is divided into the following types:

1. Traumatic (primary or secondary) - develop under the influence of a pathogenic agent, included in the number of direct necrosis.
2. Ischemic ones occur due to problems with peripheral circulation, thrombosis, low oxygen content in the blood, and blockage of blood vessels.
3. Allergic diseases are included in the group of indirect necrotic lesions. This type of illness occurs due to the body’s individual reaction to irritants.
4. Toxigenic develop under the influence of toxic substances different types.
5. Trophoneurotic lesions appear due to malfunctions of the central or peripheral nervous system and provoke disturbances in the innervation of the skin or internal organs.

Symptoms

The onset of irreversible death of body structures is characterized by tingling, numbness in the legs or arms, and loss of sensation in the damaged area. In addition, the patient's skin becomes pale and shiny. Over time, due to the cessation of blood circulation, it first becomes bluish, later dark green and even black. If the necrotic lesion is caused by poisoning, then general health the patient may worsen, nervous system become exhausted. Additionally, the patient experiences rapid fatigue.

In order to take timely measures, you need to pay attention to the first signs of the disease. The main symptoms of death of skin, bones or internal organs are presented below:

• loss of sensation;
• hyperemia of the skin;
• numbness;
• coldness in the extremities;
• swelling;
• convulsions;
• dyspnea;
• change in respiratory rhythm;
• general weakness;
• permanent increase in body temperature;
• loss of appetite;
• trophic ulcers;
• increase in heart rate.

Stages

By their nature, necrotic lesions are a terrible disease. The disease occurs in several stages, each of which has its own characteristic features. Below are the stages of development of the pathological condition:

1. Paranecrosis (or cell death). At this stage, the dying process is reversible, provided that proper treatment. Timely health care can prevent the development of complications.
2. Necrobiosis. At this stage, the destruction process already becomes irreversible. With necrobiosis, tissue metabolism is disrupted, new healthy cells are not formed.
3. Dieback. If apoptosis is a natural, genetically determined death, then cell death in this case occurs under the influence of pathogenic factors and has negative consequences for the body.
4. Autolysis. At this stage, complete decomposition of the dead structures of the body occurs. The process is started by enzymes secreted by dead cells.

Diagnostics

In order to provide qualified assistance to the patient and start treatment on time, it is important to determine where the necrotic tissue and what is the scale of the problem. For these purposes The following medical diagnostic methods are used:

• CT scan;
• radiography;
• Magnetic resonance imaging;
• radioisotope scanning.

The presented types of studies help determine the exact location of the affected area, its size, and features. By identifying characteristic changes, the stage and form of the disease, staging accurate diagnosis doctors can prescribe effective treatment to the patient. Superficial necrotic lesions are not difficult to diagnose. These include gangrene of the limbs and so on. The development of this disease is determined by the patient’s complaints, the presence of bluish or green skin in the affected area.

Treatment of tissue necrosis

Timely diagnosis and identification of the cause of necrosis are important components of successful therapy. This disease requires immediate hospitalization of the patient. Drug therapy for tissue necrosis is usually aimed at restoring blood flow. If necessary, detoxification therapy may be carried out and antibiotics may be prescribed. In difficult cases, the patient is sent for surgery.

Skin necrosis on initial stages can be treated at home. For this, the following effective traditional medicines are used:

• chestnut fruit baths;
• oak bark ash;
• lard ointment
• slaked lime.

Therapy for dry necrosis

Depending on the type of disease, therapy may vary. Dry necrosis is treated in two stages. The first is to dry the tissues, restore blood circulation and prevent further spread of the disease. The area near the area affected by necrosis is treated with an antiseptic. After disinfecting the area, apply a bandage soaked in Boric acid, ethyl alcohol or Chlorhexidine. During the first stage of therapy, the tissues affected by necrosis are dried. To do this, they are treated with a solution of potassium permanganate or brilliant green.

The second stage involves excision of non-viable tissue. Depending on the degree of necrotic lesion, the patient may have his foot cut off or undergo resection of the phalanx. All manipulations should be aimed at restoring blood circulation in damaged organs. In addition, it is important to exclude the cause that provoked the disease. To avoid bacterial infection of dead tissue, the patient is prescribed antibacterial therapy. Otherwise possible serious complications, even death.

Therapy for wet necrosis

In cases with necrotic lesions of the wet type, treatment is prescribed taking into account the degree of damage to the organ. This type of pathological condition is more dangerous for humans. Doctors on initial stage They are trying to convert wet necrosis into dry necrosis. The early stages of the disease allow this to be done. If it is not possible to change the discharge of necrosis, the patient is sent for surgery.