Nasal tissue necrosis symptoms. Tissue necrosis: causes, treatment

Necrosis is an irreversible process of necrosis of the affected tissues of a living organism as a result of external or internal factors. Such pathological condition extremely dangerous for humans, fraught with the most serious consequences and requires treatment under the supervision of highly qualified specialists.

Causes of necrosis

Most often lead to the development of necrosis:

• injury, injury, exposure to low or high temperature, radiation;
• exposure to the body of allergens from the external environment or autoimmune antibodies;
• impaired blood flow to tissues or organs;
• pathogenic microorganisms;
• exposure to toxins and some chemical substances;
• non-healing ulcers and bedsores due to impaired innervation and microcirculation.

Classification

There are several classifications of necrotic processes. According to the mechanism of occurrence, the following forms of tissue necrosis are distinguished:

1. Direct (toxic, traumatic).
2. Indirect (ischemic, allergic, trophoneurotic).

Classification by clinical manifestations:

1. Colliquation necrosis (necrotic tissue changes are accompanied by edema).
2. Coagulative necrosis (complete dehydration of dead tissue). This group includes the following types of necrosis:
   • caseous necrosis;
   • Zenker's necrosis;
   • fibrinoid necrosis of connective tissue;
   • fat necrosis.
3. Gangrene.
4. Sequester.
5. Heart attack.

Symptoms of the disease

The main symptom of the pathology is the lack of sensitivity in the affected area. With superficial necrosis, color changes skin- first, the skin turns pale, then a bluish tint appears, which can change to green or black.

When defeated lower extremities the patient may complain of lameness, convulsions, trophic ulcers. Necrotic changes internal organs lead to deterioration general condition the patient, the functioning of individual body systems (CNS, digestive, respiratory, etc.)

With colliquation necrosis, the process of autolysis is observed in the affected area - decomposition of tissues under the action of substances secreted by dead cells. As a result of this process, capsules or cysts filled with pus are formed. The most characteristic picture of wet necrosis for tissues rich in fluid. An example of colliquative necrosis is cerebral ischemic stroke. Diseases accompanied by immunodeficiency (oncological diseases, diabetes mellitus) are considered predisposing factors for the development of the disease.

Coagulative necrosis usually occurs in tissues poor in fluid but containing significant amount protein (liver, adrenal glands, etc.). The affected tissues gradually dry out, decreasing in volume.

• With tuberculosis, syphilis, some other infectious diseases necrotic processes are characteristic of internal organs, the affected parts begin to crumble (caseous necrosis).
• In Zenker's necrosis, the skeletal muscles abdomen or thighs pathological process usually start causative agents of typhoid or typhus.
• At fat necrosis irreversible changes in adipose tissue occur as a result of injury or exposure to enzymes of damaged glands (for example, in acute pancreatitis).

Gangrene can affect both individual parts of the body (upper and lower limbs) and internal organs. The main condition is the obligatory connection, direct or indirect, with external environment. Therefore, gangrenous necrosis affects only those organs that, through anatomical canals have access to air. The black color of dead tissue is due to the formation of a chemical compound of iron, hemoglobin and hydrogen sulfide. environment.

There are several types of gangrene:

• Dry gangrene - mummification of affected tissues, most often develops in the limbs due to frostbite, burns, trophic disorders in diabetes or atherosclerosis.
• Wet gangrene usually affects the internal organs when infected tissues are infected, has signs of colliquat necrosis.
• Gas gangrene occurs when necrotic tissue is damaged anaerobic microorganisms. The process is accompanied by the release of gas bubbles, which is felt on palpation of the affected area (symptom of crepitus).

Sequestration most often develops in osteomyelitis, is a fragment of dead tissue, freely located among living tissues.

A heart attack occurs due to a violation of blood circulation in a tissue or organ. The most common forms of the disease are myocardial and cerebral infarction. It differs from other types of necrosis in that necrotic tissues in this pathology are gradually replaced connective tissue, forming a scar.

Outcome of the disease

In a favorable case for the patient, the necrotic tissue is replaced with bone or connective tissue, and a capsule is formed that limits the affected area. Extremely dangerous necrosis is vital important organs(kidneys, pancreas, myocardium, brain), they often lead to death. The prognosis is also unfavorable for purulent fusion of the focus of necrosis, leading to sepsis.

Diagnostics

If there is a suspicion of necrosis of internal organs, the following types instrumental examination:

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

Using these methods, you can determine the exact location and size of the affected area, identify characteristic changes in the structure of tissues to establish an accurate diagnosis, form and stage of the disease.

Superficial necrosis, such as gangrene of the lower extremities, is not difficult to diagnose. The development of this form of the disease can be assumed on the basis of the patient's complaints, cyanotic or black color of the affected area of ​​the body, lack of sensitivity.

Treatment of necrosis

With necrotic changes in tissues, hospitalization in a hospital for further treatment is mandatory. For a successful outcome of the disease, it is necessary to correctly establish its cause and take timely measures to eliminate it.

In most cases assigned drug therapy aimed at restoring the blood flow of the affected tissues or organ, if necessary, antibiotics are administered, detoxification therapy is carried out. Sometimes it is possible to help the patient only by surgery, by amputating part of the limbs or excising dead tissues.

In the case of skin necrosis, you can quite successfully use the means traditional medicine. Effective in this case are baths from a decoction of chestnut fruits, ointment from lard, slaked lime and oak bark ash.

Intestinal necrosis is a condition in which tissues begin to die and lose their properties. Such a process is most often not reversible, and if tissue necrosis has already occurred, then it will not be possible to restore the lost area. Therefore, such a pathology should be treated in the early stages so that it is possible to save a person.

The causes of necrosis are varied, and may be the result of an illness or an independent factor that has developed for its own reasons.

Types of necrosis

The intestine can be affected in different ways, depending on how the necrotic area looks, on the location of necrosis, and the amount of dead tissue. Therefore, the following types of necrosis are distinguished:

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Causes

The causes of intestinal necrosis can be the following factors:

1. Intestinal obstruction, which is caused by prolonged accumulation of feces due to torsion of the intestines. Small intestine is less likely to undergo such pathology than the thick one. With a significant physical activity the large intestine can be strongly squeezed, which will block the access of blood.
2. Violations in the work of the central nervous system that cause destruction of the walls of the intestine.
3. Circulatory disorders in the intestinal walls can be caused by thrombosis (clots form in the intestinal vessels themselves, or migrate from other organs) or embolism (air entering the bloodstream).
4. The defeat of the intestinal tract by pathogenic microorganisms often causes necrosis in babies (especially infants). Their weakened body cannot fight infection, and therefore bacteria and viruses begin to destroy the intestinal walls very quickly.
5. Allergic response of the body to the presence foreign bodies may cause necrosis.
6. Chemical poisoning can also provoke necrosis of the tissues of the intestinal tract.
7. When operations are performed on the stomach, the consequence (complication) may be that the part of the intestine closest to the stomach begins to die.

Symptoms

Signs of intestinal necrosis often appear when the process is irreversible or slightly reversible, and therefore you need to know the symptoms of necrosis and immediately call ambulance otherwise the consequences of delay can be fatal for a person.

Symptoms of necrosis are as follows:

• severe weakness, loss of strength;
• rise in temperature;
• the pulse quickens, and the pressure drops;
• pallor and dryness of the skin;
• dry mouth;
• thirst;
• weight loss;
• appetite decreases;
• nausea and vomiting appear;
• on the late stages there are pains in the abdomen, and there is blood in the stool.

Diagnostics

When applying for medical care the patient will first palpate the abdomen.

With bowel necrosis, there will be abnormally soft parts of the abdomen. To confirm the diagnosis appoint:

• x-ray of the intestine;
• angiography or MRI;
• radioisotope scanning;
• dopplerography ( ultrasound procedure intestinal arteries)
• colonoscopy;
• diagnostic laparoscopy.

According to the results of the studies, if necrosis is detected, the patient is urgently sent to the surgical department for emergency care. If the cause of the pathology is not eliminated in time and the work of the intestine is not restored, then the patient will die.

Treatment

Treatment of intestinal necrosis is carried out in the following areas:

1. conservative therapy.
2. Relief therapy.
3. Surgical intervention.

The first two directions are mandatory, but the operation is prescribed according to indications, but since necrosis on early stage are detected only in small quantities, then most patients will still need it.

Conservative therapy

A patient with necrosis is administered:

• antibiotics;
• protein solutions;
• anticoagulants;
• electrolytes.

All this is done to reduce blood clotting, reduce thrombosis, eliminate infection and maintain the body.

Relief Therapy

To reduce the load on the intestines, the patient is washed with the stomach and the entire intestinal tract from all sides. If there is no accumulation of feces and undigested food, then the likelihood of vascular squeezing will decrease. They may also intubate a thick or small intestine, bringing the tube to the front wall of the abdomen, which will allow further feces to be removed through it.

Surgical intervention

Most patients are shown resection of the intestine (necrotic part), but even this does not always give a chance for survival. The damaged part of the intestine is removed for the patient and the healthy ones are sutured, if this is not possible, then the colostomy is removed.

Laparoscopy may help if the necrosis has just begun. Then such a small operation will eliminate the resulting defect without a full-fledged operation, which will significantly reduce the risk of infection.

Forecast

The prognosis after surgery is not very encouraging, even bowel resection does not save half of the patients. If helped conservative methods and there is a chance to restore damaged areas, then the survival rate is greater.

But this is only at an early stage of the disease, and only a few seek help during such a period.

For everyone else, the chances of recovery are less than 50%, of which another 30% may develop complications.

Prevention

It is impossible to prevent necrosis and protect yourself for life. It is important to monitor your diet and lifestyle, not to start any diseases and treat them in time, listen to doctors and follow all their prescriptions for the treatment of a particular pathology in order to prevent drug poisoning, play sports and monitor your weight.

These banal rules will not only reduce the risk of many diseases, but will also make you feel lighter and happier.

The term necrosis means the complete death of a cell. complete damage cell structure. Can cause membrane defects that cause uncontrolled leakage of cell contents into its environment.

Often, infection is the reason for the accumulation of acid metabolism products, which leads to the irreversible destruction of protein structures in the cytoplasm. The final result and reaction of the body is inflammation.

Also under the influence of necrosis, destroyed cell nucleus, and the chromatin contained in it is broken into separate parts. At the same time, it begins to shrink cell membrane. Ultimately, karyolysis occurs - the complete death of the nucleus.

Thus, necrosis describes the breakdown and death of cells seen under a microscope. However, the term itself is most often used to refer to dead tissue, the destruction of which can be seen with the naked eye.

Necrosis consists of several layers. The top layer is firm and has the texture of leather. This is followed by a granular layer, the granules of which do not exceed 0.6 mm. The bottom layer reaches the healthy area while maintaining necrosis.

Dead cells are used as dead tissue, thus providing a good breeding ground for bacteria - thanks to this feature, the spread of various microbes and pathogens almost always occurs.

Causes of the disease

The main cause is inflammation, which can be triggered by various environmental influences or lack of nutrients and oxygen.

Additional factors include:

• radioactive radiation.
• Colds.
• Toxins.
• Infection with viruses, bacteria, fungi.
• Mechanical impact
• Lack of oxygen.

Depending on which area is affected, a scar will form in that area. At severe stages necrosis, the dead area dries up completely and dies.

Also, circulatory disorders can be the root cause for the development of tissue necrosis. These factors can provoke the death of individual cells, which can ultimately cause inflammatory response in the surrounding tissues.

Secondary gangrene can also be caused by bacteria. This is especially true for poorly perfused limbs, the complications of which may also accompany occlusive diseases of the vessels and arteries.

Symptoms

Often, infected areas become red, swollen, and feel warm. Inflammation usually remains around the dying part and thus the patient may feel tense. With the death of bone and joint cells, movement restrictions almost always appear. In many cases, sensitivity in infected areas is reduced.

According to the method of exposure, cell death can be superficial and affect the skin, in more severe cases, damage to internal organs occurs. The outcomes of necrosis are manifested as black and yellow discoloration of tissues.

In case of internal deadness, pains and other associated symptoms occur:

• Heat.
• Chills.
• Dizziness.
• Nausea.

Also, when organs are affected, specific symptoms indicating the disease of the corresponding organ. Also available pain symptoms in the infected area.

Less perfused tissue is rapidly damaged, gradually acquiring a bluish tint, which eventually leads to its complete death.

Types of necrosis

Doctors distinguish different forms necrosis. For example, a severe circulatory disorder, such as peripheral arterial occlusive disease in the leg, can cause gangrene of the toes.

Necrosis refers to various processes that often lead to the destruction and death of cells. Due to this feature, there different types diseases:

• coagulation type. First of all, it is distinguished by the dark contour of the infected tissue. Within a few days after the onset of necrotic changes, residual stability occurs.
• Colliquation type. Occurs in tissues low content collagen and high content fat, especially in the brain and pancreas.
• fat type. Differs in the destruction of adipose tissue and fat cells. In this type, the collagen structure is corroded in the infected area. Occurs in connective tissue or smooth muscle - especially when autoimmune diseases.
• hemorrhagic type. calls heavy bleeding the affected area.
• Gangrene. It is a special form of coagulation type. Usually occurs after prolonged or absolute ischemia and is characterized by shrinkage of the tissue, as well as the appearance of a black tint.

Types of infection differ in the main mechanism of tissue necrosis, which is always localized, so it covers only a part of the cells.

Necrosis I Necrosis (necrōsis, Greek nekrōsis necrosis)

necrosis of cells and tissues in a living organism, accompanied by an irreversible cessation of their functions. N. is not only, but also a necessary component of the normal life of cells and tissues in the process of physiological regeneration. N. is characterized certain changes cells and intercellular substance. As a result of the activation of hydrolytic enzymes of lysosomes, the cell shrinks, concentrates in it (), then the nucleus breaks up into clumps () and dissolves (). In the cytoplasm of the cell, protein coagulation also occurs, which is replaced by the disintegration of the cytoplasm (), and then its melting (). N. can capture part of the cell (N.), or the entire cell ().

In the intercellular substance during N. depolymerization of glycosaminoglycans occurs, it is impregnated with blood plasma proteins, swells and undergoes lysis. Fibrous structures also swell and become impregnated with plasma proteins. Fibrinoid N. develops in collagen fibers, they disintegrate and dissolve. Swollen elastic fibers disintegrate and melt (). Reticular fibers disintegrate later than other fibrous structures, and the remnants of cells and intercellular substance undergo phagocytosis.

Some necrotic tissues become flabby and melt (), others thicken and dry out (). With the putrefactive fusion of such tissues, an unpleasant one appears, and they also change. N.'s sites of internals become white-yellow or are impregnated with blood, getting dark red color. Dead tissues of organs associated with the external environment, as a result of the interaction of blood pigments impregnating them with air, acquire a dirty brown, black or gray-green color.

Among complex mechanisms N. of leading importance is the factors causing N. and the duration of their action on tissues, the structural and functional features of the organs that have undergone N., the level of metabolism in them, as well as. The rate of development of N. depends on the combination of these factors. There are direct N., due to the direct action of the pathogenic factor on cells and tissues, and indirect N., arising indirectly through the vascular. nervous and endocrine systems.

N.'s reasons can be exogenous and endogenous influences. Among the exogenous causes are mechanical, high or low temperature, the action of various chemicals, microorganisms, ionizing radiation, etc. Endogenous causes N. there can be disturbances of vascular, trophic, metabolic and allergic character. Depending on the cause and conditions of N.'s development, as well as on the structural and functional characteristics of the organ in which it develops, several clinical and morphological forms of N. are distinguished: coagulation (dry), colliquative (wet), gangrene, and infarction.

Coagulation N. is based on the processes of protein denaturation with the formation of sparingly soluble compounds. In this case, the tissues are dehydrated and compacted. This form of N. occurs in tissues rich in proteins and poor in fluid, such as the kidneys, spleen, and muscles. Coagulation is curdled (caseous) N. in tuberculosis ( rice. one ), leprosy, fibrinoid N. at allergic diseases and etc.

Kollikvatsionny N. develops in the fabrics rich with liquid, for example in a brain. The melting of dead masses in the focus of dry N. is called secondary colliquation.

Gangrene - necrosis of tissues in contact with the external environment and acquiring a gray-brown or black color.

Sequester - a section of necrotic, usually bone, tissue that has not undergone autolysis. Purulent develops around the sequester.

A heart attack is one of the types of N., which develops as a result of a sudden violation of blood circulation in a part of an organ ( rice. 2 ).

At favorable outcome N. occurs in necrotic masses or N.'s area is overgrown with connective tissue and encapsulated. With dry N., calcium salts () can be deposited in dead masses. Sometimes, at the site of the focus, N. is formed (). Around the foci of colliquation N. is formed, the dead masses dissolve and arise. Necrotic parts of organs can be rejected ().

N.'s outcome is determined by the functional value of the dying part of the organ. In one cases N. of fabrics does not leave essential consequences, in others leads to serious complications.

Bibliography: Davydovsky I.V. General human, with. 156, Moscow, 1969; General pathology man, ed. A.I. Strukov and others, p. 116, M., 1982.

Stained with hematoxylin and eosin; ×250">

Rice. 1. Microslide of tuberculous granuloma with caseous necrosis in the center. Stained with hematoxylin and eosin; ×250.

II Necrosis (necrosis; Greek nekrosis necrosis,)

irreversible cessation of vital activity of tissues of a certain part of a living organism.

Allergic necrosis(n. allergica) - N. sensitized tissues when exposed to a specific allergen, such as the Arthus phenomenon.

Wet necrosis(n. humida; . N. colliquative) - N., accompanied by softening (lysis) of the affected tissues: observed in tissues rich in fluid.

Necrosis waxy(n. ceroidea; synonym: waxy, vitreous dystrophy, Zenker necrosis) - dry N. muscles, in which the foci have a gray-yellow color with a greasy sheen, i.e. have a resemblance to wax; observed in some infectious diseases (abdominal and), injuries, convulsive conditions.

Necrosis hemorrhagic(n. haemorrhagica) - N., accompanied by soaking of the affected tissues with blood.

Fat necrosis(n. adiposa; synonym adiponskrosis) - N. adipose tissue; occurs under the influence of lipolytic enzymes.

Necrosis ischemic(n. ischaemica: sleep. N.) - N., due to insufficiency of local blood circulation.

Caseous necrosis(n. caseosa) - see Caseous necrosis .

Necrosis coagulation- see Dry necrosis .

Colliquated necrosis(n. colliquativa: lat. colliquesco to liquefy) - see Wet necrosis .

Necrosis of the renal cortex, bilateral(n. corticis renurn bilateralis) - see Necrosis of the kidneys cortical .

Necrosis of the renal cortex is symmetrical(n. corticis renum symmetrica) - see Cortical necrosis of the kidneys .

Aseptic bone necrosis(osteonecrosis aseptica; synonym: avascular, osteonecrosis) - ischemic N. of the bone area: it develops more often in the epiphyses of tubular bones.

Acute radiation necrosis(n. radialis acuta) - N. l., arising a few weeks after exposure.

late radiation necrosis- N. l., which occurs many years after exposure.

Early radiation necrosis- N. l., which occurs several months after exposure.

Necrosis maranthic(n. marantica; Greek marantikos fading, weak) - N. tissues under pressure; in debilitated patients leads to the development of bedsores.

Necrosis neurogenic(n. neurogena) - see neurotic necrosis .

Necrosis neurotic(n. neurotica: syn. N. neurogenic) - N., caused by a violation of the nervous trophism; observed in some diseases of the nervous system.

Necrosis indirect(n. indirecta) - N., not associated with the direct action of the damaging factor on.

Cortical necrosis of the kidneys(n. renum corticalis; synonym: N. cortex of the kidneys, N. cortex of the kidneys symmetrical) - bilateral N. of the cortical layer of the kidneys with the preservation of the intermediate zone and pyramids; manifested by acute renal failure; observed, for example, in severe shock.

Medullary necrosis of the kidney(n. renis medullaris; syn.) - N. renal pyramid; develops as one of the complications of purulent pyelonephritis.

Necrosis direct(n. directa) - N., due to the direct action of the damaging factor on the tissue.

Dry necrosis(n. sicca; synonym: coagulation, N. coagulation) - N., characterized by tissue dehydration with denaturation and coagulation of tissue proteins.

Necrosis curdled(n. caseosa; synonym:, N. caseous) - dry N. with the formation of protein denaturation products that are not hydrolyzed for a long time and look like cottage cheese.

Necrosis traumatic secondary(n. traumatica secundaria) - H, damaged tissues, due to the development of inflammatory, vascular and other secondary changes in them.

Details

Necrosis- necrosis, death of cells and tissues in a living organism, while their vital activity completely stops.

The necrotic process goes through a series stages :

1. paranecrosis - reversible changes similar to necrotic
2. necrobiosis - irreversible dystrophic changes(while catabolic reactions predominate over anabolic)
3. cell death
4. autolysis - decomposition of a dead substrate under the action of hydrolytic enzymes and macrophages

Microscopic signs of necrosis:

1) Kernel changes

1. Karyopyknosis- wrinkling of the nucleus. At this stage, it becomes intensely basophilic - stained dark blue with hematoxylin.
2. Karyorrhexis- disintegration of the nucleus into basophilic fragments.
3. Karyolysis- dissolution of the nucleus

Pycnosis, rexis and lysis of the nucleus follow one after another and reflect the dynamics of activation of proteases - ribonuclease and deoxyribonuclease. When fast developing necrosis the nucleus undergoes lysis without the stage of karyopyknosis.

2) Changes in the cytoplasm

• plasma coagulation. First, the cytoplasm becomes homogeneous and acidophilic, then protein coagulation occurs.
• plasmorhexis
• plasmolysis

Melting in some cases captures the entire cell (cytolysis), and in others - only a part (focal colliquational necrosis or balloon dystrophy)

3) Changes in the intercellular substance

a) collagen, elastic and reticulin fibers swell, being impregnated with plasma proteins, turn into dense homogeneous masses, which either undergo fragmentation, or clumpy disintegration, or lyse.

The breakdown of fibrous structures is associated with the activation of collagenase and elastase.

Reticulin fibers do not undergo necrotic changes for a very long time, therefore they are found in many necrotic tissues.

b) the intermediate substance swells and melts due to the depolymerization of its glycosaminoglycans and impregnation with blood plasma proteins

With tissue necrosis, their consistency, color and smell change. The tissue may become dense and dry (mummification), or it may become flabby and melted.

The fabric is often white and has a white-yellow color. And sometimes it is dark red when it is saturated with blood. Necrosis of the skin, uterus, skin often acquires a gray-green, black color.

causes of necrosis.

Depending on the cause of necrosis, the following types are distinguished:

1) traumatic necrosis

Is the result of direct action on the tissue of physical and chemical factors (radiation, temperature, electricity, etc.)

Example: when exposed to high temperatures, tissue burns occur, and when exposed to low temperatures, frostbite occurs.

2) toxic necrosis

It is the result of the direct action of toxins of bacterial and non-bacterial origin on tissues.

Example: necrosis of cardiomyocytes under the influence of diphtheria exotoxin.

3) trophoneurotic necrosis

Occurs when the nervous tissue trophism is disturbed. The result is a circulatory disorder, dystrophic and necrobiotic changes that lead to necrosis.

Example: bedsores.

4) allergic necrosis

It is an expression of an immediate hypersensitivity reaction in a sensitized organism.

Example: the Arthus phenomenon.

5) vascular necrosis– heart attack

Occurs when there is a violation or cessation of blood flow in the arteries due to thromboembolism, prolonged spasm. Insufficient blood flow causes ischemia, hypoxia and tissue death due to the cessation of redox processes.

To direct necrosis include traumatic and toxic necrosis. Direct necrosis is due to the direct influence of the pathogenic factor.

Indirect necrosis occurs indirectly through the vascular and neuroendocrine systems. This mechanism of necrosis development is typical for species 3-5.

Clinical and morphological forms of necrosis.

They are distinguished, taking into account the structural and functional features of organs and tissues in which necrosis occurs, the causes of its occurrence and the conditions for development.

1) coagulation (dry) necrosis

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 resulting dead areas are dry, dense, gray-yellow in color.

Coagulative necrosis occurs in organs rich in proteins and poor in fluids (kidneys, myocardium, adrenal glands, etc.).

As a rule, a clear boundary between dead tissue and living tissue can be clearly noted. There is a strong demarcation inflammation at the border.

Examples:

Waxy (Zenker's) necrosis (in the rectus abdominis muscles in acute infectious diseases)

heart attack

Caseous (cheesy necrosis) with syphilis, tuberculosis

Dry gangrene

Fibrinoid - necrosis of connective tissues, which is observed in allergic and autoimmune diseases. Collagen fibers and smooth muscles are severely damaged middle shell blood vessels. Characterized by loss normal structure collagen fibers and the accumulation of homogeneous necrotic material of bright pink color, which is similar (!) to fibrin.

2) colliquative (wet) necrosis

It is characterized by the melting of dead tissue, the formation of cysts. It develops in tissues relatively poor in proteins and rich in fluid. Cell lysis occurs as a result of the action of its own enzymes (autolysis).

There is no clear zone between dead and living tissue.

Examples:

Ischemic cerebral infarction

When the masses of dry necrosis are melted, they speak of secondary colliquation.

3) Gangrene

Gangrene- necrosis of tissues in contact with the external environment (skin, intestines, lungs). In this case, the tissues become gray-brown or black, which is associated with the conversion of blood pigments into iron sulfide.

a) dry gangrene

Necrosis of tissues in contact with the external environment without the participation of microorganisms. Most often occurs in the extremities as a result of ischemic coagulative necrosis.

Necrotized tissues dry out, shrivel and compact under the influence of air, they are clearly demarcated from viable tissue. On the border with healthy tissues, demarcation inflammation occurs.

Demarcation inflammation – reactive inflammation around dead tissue, which delimits dead tissue. The restriction zone, respectively, is demarcation.

Example: - limb gangrene in atherosclerosis and thrombosis

Frostbite or burns

b) wet gangrene

Develops as a result of layering on necrotic tissue changes bacterial infection. Under the action of enzymes, secondary colliquation occurs.

The tissue swells, becomes edematous, fetid.

The occurrence of wet gangrene is promoted by circulatory disorders, lymph circulation.

In wet gangrene, there is no clear distinction between living and dead tissue, which complicates treatment. For treatment, it is necessary to transfer wet gangrene to dry, only then carry out amputation.

Examples:

Gangrene of the intestine. Develops with obstruction of the mesenteric arteries (thrombi, embolism), ischemic colitis, acute peritonitis. The serous membrane is dull, covered with fibrin.

Bedsores. Bed sore - necrosis of superficial areas of the body subjected to pressure.

Noma is a watery cancer.

c) gas gangrene

Occurs when the wound becomes infected with anaerobic flora. It is characterized by extensive tissue necrosis and the formation of gases as a result of the enzymatic activity of bacteria. Frequent clinical symptom- crepitus.

4) sequester

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

Example: - sequester for osteomyelitis. A capsule and a cavity filled with pus form around such a sequester.

soft tissues

5) heart attack

Vascular necrosis, consequence and extreme expression of ischemia. The reasons for the development of a heart attack are prolonged spasm, thrombosis, arterial embolism, as well as the functional stress of the organ in conditions of insufficient blood supply.

a) forms of a heart attack

Most often, heart attacks are wedge-shaped (the base of the wedge faces the capsule, and the tip faces the gates of the organ). Such heart attacks are formed in the spleen, kidneys, lungs, which is determined by the nature of the architectonics of these organs - the main type of branching of their arteries.

Rarely, necrosis irregular shape. Such necrosis occurs in the heart, intestines, i.e., in those organs where non-main, loose or mixed type arterial branches.

b) value

A heart attack can cover most or all of an organ (subtotal or total heart attack) or is detected only under a microscope (microinfarction).

c) appearance

- white

Represents an area white-yellow color well demarcated from the surrounding tissue. Usually occurs in tissues with insufficient collateral circulation (spleen, kidneys).

- white with hemorrhagic halo

It is represented by a white-yellow area, but this area is surrounded by a zone of hemorrhages. It is formed as a result of the fact that the spasm of the vessels along the periphery of the infarction is replaced by their expansion and the development of hemorrhages. Such a heart attack is found in the myocardium.

- red (hemorrhagic)

The site of necrosis is saturated with blood, it is dark red and well demarcated. Occurs in organs where venous congestion where there is no main type of blood supply. It occurs in the lungs (because there are anastomoses between the bronchial and pulmonary arteries), intestines.

Clinical manifestations of necrosis.

1) systemic manifestations: fever, neutrophilic leukocytosis. Intracellular enzymes are determined in the blood: the MB-isoenzyme of kratinkinase increases with myocardial necrosis.

2) Local manifestations

3) Impaired function

Outcomes of necrosis:

1) demarcation

With a relatively favorable outcome, reactive inflammation occurs around the dead tissue, which delimits the dead tissue from the healthy one. In this zone, blood vessels expand, plethora and edema occur, a large number of leukocytes.

2) organization

Replacement of dead masses with connective tissue. In such cases, a scar is formed at the site of necrosis.

3) encapsulation

Fouling of the area of ​​necrosis with connective tissue.

4) petrification

Calcification. Accumulation of calcium salts in the capsule.

5) ossification

Extreme degree of petrification. Bone formation in the site of necrosis.

6) purulent fusion

Such is the purulent fusion of heart attacks in sepsis.