Treatment of soft tissue skin necrosis with medications. What is necrosis

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

The necrotic process goes through a series of stages :

1. paranecrosis - reversible changes similar to necrotic
2. necrobiosis – irreversible dystrophic changes (in this case, catabolic reactions predominate over anabolic ones)
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– core shrinkage. At this stage, it becomes intensely basophilic—it turns dark blue with hematoxylin.
2. Karyorrhexis– disintegration of the nucleus into basophilic fragments.
3. Karyolysis– core dissolution

Pyknosis, rhexis and nuclear lysis occur sequentially one after another and reflect the dynamics of activation of proteases - ribonuclease and deoxyribonuclease. With rapidly developing necrosis, the nucleus undergoes lysis without the stage of karyopyknosis.

2) Changes in the cytoplasm

• plasmacoagulation. First, the cytoplasm becomes homogeneous and acidophilic, then protein coagulation occurs.
• plasmorrhexis
• plasmolysis

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

3) Changes in the intercellular substance

A) collagen, elastic and reticulin fibers swell, saturated with plasma proteins, transform into dense homogeneous masses, which either undergo fragmentation, or clumpy decay, or are lysed.

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, and therefore are found in many necrotic tissues.

b) the interstitial substance swells and melts due to 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 soaked in blood. Necrosis of the skin, uterus, and skin often becomes gray-green or black.

Causes of necrosis.

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

1) traumatic necrosis

It is the result of a direct effect on the tissue of physical chemical factors(radiation, temperature, electricity, etc.)

Example: when exposed high temperature tissue burns appear, 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 tissue.

Example: necrosis of cardiomyocytes when exposed to diphtheria exotoxin.

3) trophoneurotic necrosis

Occurs when there is a violation of the nervous trophism of tissues. 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: Arthus phenomenon.

5) vascular necrosis– heart attack

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

TO direct Necrosis includes traumatic and toxic necrosis. Direct necrosis is caused by the direct influence of a 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 characteristics of the organs and tissues in which necrosis occurs, the reasons for its occurrence and the conditions of development.

1) coagulation (dry) necrosis

Dry necrosis is based on the processes of protein denaturation with the formation of sparingly soluble compounds that can long time do not undergo hydrolytic degradation.

The dead areas that appear are dry, dense, gray-yellow in color.

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

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

Examples:

Waxy (Zenker's) necrosis (in the rectus abdominis muscles during 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 of the middle lining of blood vessels are severely damaged. It is characterized by the loss of the normal structure of collagen fibers and the accumulation of homogeneous necrotic material of a bright pink color, which is similar (!) to fibrin.

2) liquefaction (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 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 masses of dry necrosis melt, they speak of secondary colliquation.

3) Gangrene

Gangrene– necrosis of tissues in contact with external environment(skin, intestines, lungs). In this case, the tissues become gray-brown or black, which is associated with the transformation 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.

Necrotic tissues dry out, shrink and harden when exposed to air, and 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, accordingly, is a demarcation zone.

Example: - gangrene of the limb with atherosclerosis and thrombosis

For 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 swollen, and foul-smelling.

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

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

Examples:

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

Bedsores. Bedsore is the death of superficial areas of the body that are subject to pressure.

Noma is a watery cancer.

c) gas gangrene

Occurs when a 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. A common clinical symptom is crepitus.

4) sequester

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

Example: - sequester in osteomyelitis. Around such a sequester a capsule and a cavity filled with pus will form.

Soft fabrics

5) heart attack

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

a) forms of heart attack

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

Less often, necrosis has irregular shape. Such necrosis occurs in the heart, intestines, i.e. in those organs where non-main, scattered or mixed type branching of arteries.

b) magnitude

An infarction may involve most or all of an organ (subtotal or total infarction) or may be detected only under a microscope (microinfarction).

c) appearance

- white

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

- white with hemorrhagic rim

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 vascular spasm along the periphery of the infarction is replaced by their expansion and the development of hemorrhages. Such an infarction is found in the myocardium.

- red (hemorrhagic)

The area of ​​necrosis is saturated with blood, it is dark red and well demarcated. It is found in those organs where venous congestion is characteristic, where there is no main type of blood supply. Occurs in the lungs (since 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 kratin kinase increases with myocardial necrosis.

2) Local manifestations

3) Dysfunction

Outcomes of necrosis:

1) demarcation

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

2) organization

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

3) encapsulation

Overgrowth 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 area of ​​necrosis.

6) purulent melting

This is the purulent melting of infarcts during sepsis.

Trophic ulcer- this is a long-term non-healing defect of the integumentary tissue on a pathological basis (with possible involvement of deeper tissues).

Reasons for the development of trophic ulcers:

1) Arterial inflow disorders:

• Obliterating atherosclerosis.
• Obliterating endarteritis.
• Aortoarteritis.
• Thrombosis, embolism, vascular damage.
• Raynaud's disease (angiospasm).
• Arteriovenous shunts.

2) Disorders of venous outflow:

• Varicose veins lower limbs.
• Acute and chronic superficial and deep thrombophlebitis.
• Postthrombophlebitic syndrome.
• Congenital anomalies.

3) Lymphatic drainage disorders:

• Consequence of recurrent erysipelas.
• Elephantiasis.
• Congenital anomalies.

4) Diseases of the nervous system:

• CNS - syringomyelia, poliomyelitis, brain tumors and spinal cord, stroke.
• PNS - paresis, paralysis, neuritis.

5) Specific infection:

• Tuberculosis.
• Leprosy (leprosy).
• Helicobacter infection.
• Syphilis.
• Actinomycosis.
• Anthrax, brucellosis, etc.

6) Decaying tumors(for example, ulcerative form of cancer, etc.)

7) Traumatic lesions:

• Burns - thermal, chemical, radiation, electrical burns.
• Extensive wounds with large necrosis of integumentary tissue.

8) Systemic diseases:

• Scleroderma.
• Systemic lupus erythematosus.

9) Violations metabolic processes:

• Hormonal imbalances: diabetes, Itsenko-Cushing's disease and syndrome.
• Hypo- and avitaminosis (for example: scurvy), hypo- and dysproteinemia, nutritional dystrophy.
• Severe anemia and other blood diseases.

Clinic

The ulcerative process is characterized by the simultaneous presence of necrosis and tissue regeneration processes in the lesion.

Skin ulcers are characterized by greater polymorphism, are less complicated by secondary infection and are not affected by enzymes.

Ulcers of the mucous membranes are under the constant influence of enzymes and various microflora, which creates conditions for their slow healing.

When examining an ulcer, pay attention to:

1). Ulcer shape: round, oval, star-shaped.

2). Localization: skin or mucous membranes, on what part of the body.

3). Dimensions (in centimeters).

4). Depth: superficial, deep, crater-shaped.

5). The edges of the ulcer: thinned, smooth, uneven, undermined, thickened, calloused (callous).

6). Nature of the discharge: serous, purulent, hemorrhagic, etc.

7). The severity of necrotic processes.

8). Presence of granulations and epithelialization.

The clinical picture of ulcers depends on the disease that led to the formation of the ulcer:

• For atherosclerosis ulcers are usually located on the lower leg and foot; they are small, round in shape, the granulations are pale, the edges of the ulcer are dense and uneven. Clinically, a weakening of the pulsation of the main vessels of the legs is determined.
• For varicose veins ulcers are usually located in the lower third of the leg, in the area of ​​the inner ankle, large, deep, slightly painful on palpation, the skin around them is sclerotic and pigmented. Clinically, varicose veins are detected.
• For postthrombophlebitic syndrome ulcers are also located in the lower third of the leg, in the area of ​​the inner ankle, but they are usually larger in size (they can cover the entire circumference of the leg). The ulcers are usually superficial with flat edges, around which there is pronounced swelling and tissue sclerosis (indurative cellulite).
• Radiation ulcers- deep (sometimes reaching the bones), round, with uneven edges, the skin around them is atrophic. The formation of radiation ulcers is usually preceded by certain skin changes: pigmentation, telangiectasia, loss of ears, gradual atrophy of the skin and sclerosis of the subcutaneous fatty tissue.
• When the tumor is ulcerated - the ulcer has dense, thickened, lumpy, uneven edges, the bottom is covered with necrotic tissue. Around the ulcer, areas of tumor growth or a dense infiltrate, fused with the surrounding tissues, are often visible.

Differential diagnosis

carried out with wounds, because they also have a defect in the integumentary tissue. However, wounds heal in no more than 2 months. If this does not happen, then regeneration slows down sharply and the process is usually called a trophic ulcer.

Trophic ulcer	Wound
Duration - more than 2 months.	Duration - less than 2 months.
No tendency to heal.	Healing proceeds according to the phases of the wound process.
Localized in the center of trophic disorders.	The surrounding tissues have a normal appearance.
Granulations are sluggish, gray-brown in color.	The granulations are bright red, “juicy”.
On the surface there is a banal microflora.	The presence of microflora is not necessary.
Covered with necrotic tissue and fibrin deposits.	Necrotic tissue and fibrin are usually absent.

In addition, long-term ulcers with calloused edges (callous ulcers) are prone to malignancy, so it is recommended to take a biopsy of several pieces of tissue and send it for histological examination.

treatment of trophic ulcers should be comprehensive and consist of general and local measures.

1). General treatment :

Aimed at eliminating the causes that led to the occurrence and development of trophic ulcers. If the root cause is not eliminated, ulcers can form in the same place within 1-2 months. Since the causes are different, there is no single treatment regimen for trophic ulcers. However, the following always apply:

• Bed rest and immobilization affected part of the body.
• Antibiotic therapy. Intra-arterial and endolymphatic administration are widely used.
• Detoxification therapy- saline and detoxification solutions (hemodesis) are used.
• Immunostimulating therapy(T-activin, thymalin, prodigiosan, levamisole).
• Vitamin therapy, good nutrition normalization of metabolic processes(retabolil, methyluracil).
• Improved blood circulation in the area of ​​trophic ulcers (reopoliglucin, detralex, etc.).
• And most importantly, the underlying disease that led to the development of the ulcer is treated.

2). Local treatment

consists of 2 stages:

• Clearing the ulcer of necrotic tissue and suppressing infection. For this purpose, staged necrectomies, dressings with antiseptics (chlorhexidine, miramistin, lavasept), proteolytic enzymes (trypsin), sorbents (polyphepan), as well as special impregnated dressings (Activtex, etc.) are used. The skin around the ulcer is treated with alcohol or iodine (to prevent infection). Physiotherapy (quartz, electrophoresis with trypsin, magnetic therapy), HBOT, ozone therapy, and vacuum therapy are successfully used. Some authors do not recommend using ointment dressings to cleanse trophic ulcers, but they have received good results when using Iruksol ointment, which has antibacterial and necrolytic effects.
• Closing a defect. With small ulcers, after its cleansing and development of granulations, independent epithelization occurs. During this phase, you can use wet-dry dressings with antiseptics, as well as ointments that stimulate epithelization (actovegin, solcoseryl, methyluracil). For small ulcers (less than 1 cm), it can be “cauterized” with a solution of brilliant green or potassium permanganate - then the ulcer will heal under the scab. For venous ulcers, an occlusive zinc-gelatin dressing with Unna paste can be used, which is applied for 1-2 months.

Surgical treatment is used when attempts to close the defect conservatively are ineffective, and includes two points:

• Excision of pathologically altered granulations and scars.
• Plastic closure of tissue defects with skin: excision of the ulcer with plastic surgery is used local tissues, plasty with a skin flap “on a leg” (Filatov’s method) or free skin plasty.

A fistula is a pathological passage in tissues that connects an organ, a natural or pathological cavity with the external environment, or organs (cavities) with each other.

Classification

1). By origin:

• Congenital(malformations) - median and lateral fistulas of the neck, umbilical fistulas, etc.
• Purchased:

Summoned inflammatory process(fistulas due to osteomyelitis, paraproctitis, tuberculosis, etc.). When infected foreign bodies(ligatures) the so-called ligature fistulas.

Caused by trauma.

Caused by the disintegration of a tumor (for example, in the ulcerative form of cancer).

Created operationally ( artificial fistulas) - stomas or interorgan anastomoses.

2). In relation to the external environment:

• External - communicates an organ, cavity or tissue with the external environment (for example, an intestinal fistula).
• Internal - communicate 2 hollow organs, or an organ with a cavity (natural or pathological).

3). Based on the lining of the fistula tract, the following are distinguished:

• Granulating- walls are covered granulation tissue. They are usually pathological. Self-healing is hampered by the presence of “aggressive” discharge (pus, digestive juices, mucus, etc.).
• Epithelized (tubular) - the walls are lined with epithelium. They are usually congenital. In this case, regeneration is complete and there is no tissue defect. That is why it is impossible to close it spontaneously.
• Labiform- the epithelium of the mucous membrane of a hollow organ directly passes onto the skin. They are usually artificial. Labial fistulas can be complete (all contents are discharged outward) and incomplete (part of the contents passes through the organ, and the other part is discharged outward). A labial fistula can only be created or cured by surgery.

4). According to the nature of the discharge:

• Purulent (for purulent diseases - osteomyelitis, paraproctitis).
• Fecal (cecostoma, colostomy, transversostomy, sigmostoma, ileostomy, etc.).
• Urinary (epicystostomy, pyelostomy).
• Biliary (cholecystostomy).
• Mucous membranes (tracheostomy).
• Salivary, liquor, etc. are very rare.

5). According to the organs and cavities that the acquired fistula connects:

• Tracheoesophageal.
• Bile-pleural.
• Vesicouterine
• Vaginal-rectal, etc.

6). Artificial fistulas are divided into:

• Ostomies, connecting the organ with the external environment and serving to relieve the organ when it is impossible to empty it normally.
• Interorgan anastomoses- applied to restore disturbed anatomical relationships after organ resection.

7). Depending on the reasons that forced an artificial fistula, there are:

• Permanent fistulas- imposed if the disease is incurable.
• Temporary fistulas- they are created by granulation with the expectation that they will subsequently heal on their own.

8). By difficulty:

simple and complex (4 degrees of structural complexity),

The clinical picture and discharge depend on the type of fistula.

1). External hole usually does not exceed a few centimeters.

2). The discharge can be different - pus, feces, urine, mucus, bile, etc.

3). The condition of the surrounding tissues depends on the type of discharge:

• With gastric and duodenal fistula, the skin around the opening is inflamed (dermatitis).
• With a urinary fistula, compaction and swelling of the surrounding tissues are observed.

4). Violation general condition : with purulent fistulas, there is an increase in temperature and symptoms of intoxication, which intensify when the outflow of pus is difficult. It's also possible secondary infection through the fistula.

5). Violations of the function of internal organs- for example, with gastrostomy and ileostomy, a violation of the water-salt and protein balance develops (due to the loss of digestive juices). Pronounced dysfunction of organs is caused by the flow into their cavity of a secretion that is not characteristic of this organ (for example: the flow of food into the bronchus, or the entry of feces bladder).

6). Flow dynamics: granulating fistulas can heal on their own if the outflow of discharge through them stops. Surgery is required to close epithelialized and labiform fistulas.

7). Additional Methods diagnosis of fistulas:

• Probing the fistula - in some cases makes it possible to determine the direction of its course.
• Fistulography - a radiopaque substance (Verografin, Omnipaque) is injected into the fistula and X-ray in 2 projections.
• After administration of contrast, an ultrasound can be performed.
• If fistulas of internal organs are suspected, contrast radiography with a barium suspension is used, which is injected into the lumen of the desired organ.
• Examination of the discharge fistula for the presence of certain substances by which the affected organ can be identified (for example, the presence uric acid characteristic of a urinary fistula).
• For fistulas of hollow organs, you can inject dye into the fistula (diamond green, methylene blue - mixed with hydrogen peroxide). In this case, the dye may appear in the contents of the organ.
• Sometimes endoscopic examination (FGDS, colonoscopy, etc.) can be used.
• In a blood test for long-term purulent fistulas, inflammatory changes can be detected; in a urine test - signs of amyloidosis (i.e. proteinuria, etc.).

However, despite this, sometimes the diagnosis of fistulas (especially internal) is made only during surgery.

If the fistula is combined with signs of inflammation, general treatment is carried out:

1). Antibiotic therapy.

2). Detoxification therapy - in the presence of intoxication.

3). General strengthening agents - vitamins, methyluracil, retabolil.

Local treatment depends on the type of fistula:

• For granulating fistulas you need to clean the channel and prevent the contents from leaking. To do this, the pathological focus is drained, creating a shorter and wider outflow path. The fistula tract is washed daily with antiseptics, after which it heals. IN in rare cases, with flaccid granulations, it is necessary to excise them and the scarred walls of the fistula tract and apply sutures.
• For epithelized fistulas the only method of treatment is surgery: after staining the fistula with a mixture of methylene blue and hydrogen peroxide, the entire epithelial lining of the fistula tract is removed and the wound is sutured.
• For lip fistulas The organ wall is mobilized and the hole in it is sutured. After this, the fistula tract is removed and the wound is sutured. In case of cicatricial changes in the walls of the organ, it is necessary to perform its resection.

Care for artificial (labial) fistulas:

• For fecal fistulas, special colostomy bags are used, which are attached to the stomach like a belt. Sometimes (for incomplete fistulas) special obturators are used that close the external opening without interfering with the movement of chyme through the intestine.
• For urinary or biliary fistulas (epicystostomy, cholecystostomy), drainage of the fistula is used with discharge of the discharge into a bottle.

To prevent irritation, the skin around fistulas of hollow organs must be treated daily with Lassara paste, silicone pastes, polymerizing film or indifferent ointment.

Necrosis is the death of tissues, organs or their parts in a living organism. Necrosis is a pathological process; it should be distinguished from the physiological renewal of body cells.

Gangrene is a special type of necrosis, which is characterized by certain symptoms:

• The fabrics have a characteristic black color with a greenish tint, which is associated with the decomposition of hemoglobin upon contact with air.
• That is why only organs that have a connection with the external environment are affected (limbs, lungs, gallbladder, intestines, etc.). In this regard, there is no gangrene of the brain, liver, or pancreas.
• The whole organ or most of it is affected. There is no gangrene of a limited part of the body (for example, the dorsum middle phalanx finger).

Etiology of necrosis

According to etiology, all non-goats can be divided into 2 groups:

1). Direct necrosis- occur at the site of impact external factor(mechanical, thermal, chemical, etc.).

2). Indirect necrosis(circulatory) - arise in connection with a violation of the nutrition of cells in a living organism. For their occurrence, it is not necessary that an external factor influence a specific area of ​​the body.

Causes of circulatory necrosis:

• Impaired arterial inflow (atherosclerosis, thrombosis, etc.).
• Violation of venous outflow or lymphatic drainage (varicose veins, elephantiasis, etc.).
• Microcirculation disorders (diabetic microangiopathy, systemic vasculitis, bedsores).
• Disturbance of innervation (nerve damage, polyneuropathy, etc.).

All necrosis can be divided into dry and wet:

Dry necrosis is formed due to chronic disruption of the blood supply to a limited area of ​​tissue. Usually these are patients with underdeveloped subcutaneous tissue. Necrosis develops as a coagulation type.

Wet necrosis are formed during acute disruption of the blood supply to a large volume of tissue (thrombosis of the main vessel). Usually these are patients with well-developed subcutaneous tissue, suffering from concomitant diseases and decreased immunity. An important factor is the addition of an infection. Necrosis develops as a colliquation type, it is deeper than coagulation.

The clinic of dry and wet necrosis is very different:

Dry necrosis	Wet necrosis
The volume of tissue decreases (due to drying).	Increased volume due to tissue swelling.
Coagulative nature of necrosis.	Colliquation nature of necrosis.
The presence of a clear line of demarcation (i.e., a boundary separating dead tissue from living tissue).	Lack of a clear boundary separating necrotic tissue from viable tissue.
No infection.	Attachment of a purulent or putrefactive infection. Expressed inflammatory reaction: swelling, hyperemia, increase in organ volume, there are blisters with purulent or hemorrhagic contents. Foul-smelling purulent exudate is released from skin defects.
No intoxication of the body.	Severe intoxication.
There are no changes in the analyzes.	Blood and urine tests show “purulent” changes.

Dry necrosis can turn into wet necrosis and vice versa.

Treatment of dry necrosis (gangrene)

is aimed at reducing the area of ​​necrotic tissue and maximizing the preservation of the organ.

1). General treatment:

• Etiotropic therapy- it is urgent to act on the cause of necrosis: for example, in case of arterial thrombosis, it is necessary to urgently perform thrombectomy or other surgery, etc.
• Vascular therapy- aimed at improving blood circulation in the affected area and “pushing” the necrosis zone to the periphery. The emphasis is on intra-arterial administration of drugs (reopolyglucin, trental, heparin, Actovegin, etc.)
• Antibiotic therapy- to prevent infection and the transition of necrosis to wet.

2). Local treatment:

• Prevention of infection: the skin around the necrosis is treated with alcohol, boric acid, chlorhexidine, miramistin or other antiseptics.
• Drying fabrics: the necrosis zone is “cauterized” with a solution of brilliant green or potassium permanganate.
• After the demarcation line is formed (usually after 2-3 weeks), an economical necrectomy or amputation. The incision line should be in the area of ​​healthy tissue, as close as possible to the demarcation line.

Treatment of wet necrosis (gangrene)

1). General treatment:

• Antibiotic therapy- 2 antibiotics and Metrogyl are prescribed, which are administered intravenously, intramuscularly, and also (necessarily) intra-arterially (by puncture or catheterization of the arteries).
• Intensive Vascular Therapy(reopolyglucin, novocaine, actovegin, trental, heparin, nicotinic acid, detralex, etc.).
• Detoxification therapy- hemodez, polyglucin, extracorporeal detoxification methods - hemosorption, ultraviolet and laser irradiation of blood, electrochemical oxidation of blood (intra-arterial administration of sodium hypochlorite). HBO is widely used.
• Correction of impaired organ functions.

2). Local treatment:

In the early stages, in the absence of an immediate threat to life, it is done an attempt to convert wet necrosis into dry. To do this, at each dressing, the wound is washed with hydrogen peroxide, the purulent leaks are opened and drained, a necrectomy is performed and bandages with antiseptics (chlorhexidine dioxidine, miramistin) and proteolytic enzymes (trypsin) are applied. You can use “cauterizing” antiseptics (potassium permanganate). Most surgeons do not recommend using ointments during this period.

If the effect is successful (which happens quite rarely), dry necrosis is treated.

If, against the background of local and general treatment, swelling does not subside within 1-2 days, inflammation does not subside, the process spreads further, intoxication persists or progresses, this is an indication for emergency surgery to save a life.

The operation consists of removing necrotic tissue or organs within known healthy tissue. Amputations are performed by retreating some distance from the necrosis zone. More precisely, the level of amputation can be selected based on data from functional tests and instrumental research methods: Dopplerography, rheovasography, thermography, angioscintigraphy, polarography, etc.

Bedsores

A bedsore is a necrosis of soft tissues that develops when they are compressed as a result of circulatory disorders. In this case, soft tissues are compressed between the bony protrusions of the body and the bed ( exogenous bedsores). Bedsores often form in weakened patients (sepsis, cancer, chronic debilitating diseases) who lie in bed for a long time without moving. Sometimes bedsores occur due to even minor compression as a result of severe neurotrophic changes fabrics ( endogenous bedsores).

The most common localization of bedsores: on the shoulder blades, sacrum, back of the head, heels, greater trochanter, elbows. Sometimes bedsores also form in internal organs (gall bladder, intestines, trachea) as a result of pressure on their walls (stones, drains, etc.). Sometimes bedsores are formed from compression of tissue with a plaster cast, transport bus or a tourniquet.

The following factors predispose to the development of bedsores::

• Disorder of blood circulation in tissues due to compression of blood vessels.
• Disturbance of innervation (for example: with spinal cord injury).
• Infection - bedsores often form due to fecal fistulas, when constant irritation and infection of the skin occurs.

1). The first signs of the development of a bedsore are symptoms of local circulatory disorders: pale skin, and then cyanosis.

2). Then swelling of the skin appears, detachment of the epidermis and the formation of small or large blisters filled with hemorrhagic contents.

3). Soon the blisters burst, leaving behind red or purple ulcerative surfaces.

4). At the site of the ulcers, necrosis develops, which spreads throughout the entire depth of the tissue (sometimes reaching the bone), as well as in width. The size of necrosis sometimes reaches ten centimeters. Necrosis can be dry (in the absence of infection) or wet (in the presence of infection).

The development time of bedsores can range from 1 to several days.

1). General treatment is aimed at eliminating predisposing factors (treatment of sepsis, normalization of blood circulation and innervation in the lesion, vitamin therapy, etc.).

2). Local treatment consists of staged necrectomies, which are performed both surgically and chemically (proteolytic enzymes). After removing all necrotic tissue and cleansing the wound surface, the wound is treated with ointments that accelerate regeneration and epithelization (sorcoseryl, actovegin).

Prevention

1). Proper patient care:

• Periodically turn patients in bed.
• Place inflatable rubber rings under the bony protrusions.
• Remove wrinkles from bedding.
• The skin in places where bedsores most often form is wiped 2 times a day with a solution of camphor or salicylic alcohol, cologne and sprinkled with talcum powder.
• Careful toileting of patients with impaired function is necessary pelvic organs and external fistulas.

2). Drains should be removed promptly.

3). When treating fractures with a plaster cast, constant monitoring of the patient is necessary - if pain occurs, the bandage should be removed.

4). If long-term mechanical ventilation is necessary, it is not carried out through an endotracheal tube, but a tracheostomy is applied.

Description:

Necrosis (death) is the local death of cells, tissues or organs in a living organism; death can occur from direct destruction by a traumatic agent, from a circulatory disorder or a trophic disorder.

Symptoms:

Clinical variants of neurosis:
      * Coagulation necrosis (dry)
      * Liquation necrosis (wet)
      * Caseous necrosis
      * Sequester (medicine)
      * Gangrene
      * Heart attack
      * Bedsores

Causes:

Factors leading to necrosis are: mechanical, thermal, electrical, chemical, toxic, radiation, etc.

The impact on cells, tissues and organs of mechanical force that exceeds the resistance of the membranes leads to their softening, ruptures, etc. Temperatures above +60 degrees C or below -15 degrees C cause,. At the places where high voltage electric current enters and exits the body, a very high temperature develops, and “signs of current” appear on the body - tissue burned in these places.

Chemical action. Strong acids, coagulating cell proteins, cause dry necrosis. Strong alkalis, dissolving proteins and saponifying fats, lead to the development of colliculative tissue necrosis (both). Microbial toxins can also lead to necrosis of cells and tissues (for example, anaerobic gangrene of the limb, etc.).

Circulatory disorders that cause necrosis of tissues or organs are caused by for the following reasons: a) disturbance of cardiac activity, its weakening (decompensation); b) prolonged spasm or obliteration of blood vessels (vascular sclerosis with senile gangrene, obliterating chpdarteritis and gangrene with ergot poisoning, etc.); c) compression or injury to a vessel (necrosis of the intestine with a strangulated hernia, gangrene of a limb if the tourniquet is not removed in a timely manner or is excessively tight plaster cast); d) disturbance of blood chemistry, leading to thrombosis of the main vessel in the absence of sufficiently developed collaterals (thrombosis, embolism).

Circulatory disorders and subsequent necrosis often determine the course of surgical and other diseases. Thus, tissue necrosis plays a big role in the development of the clinic anaerobic gangrene, obliterating endarteritis, gangrenous, acute, intestinal obstruction, strangulated hernias, perforated gastric ulcer, etc.

Violations of tissue trophism can also lead to necrosis even with the most minor external influences. An example is the rapid development on the body during spinal cord injuries.

Treatment:

For treatment the following is prescribed:

The elements of complex treatment are improving the general condition of the patient, stimulating immunobiological forces and regenerative properties, symptomatic therapy, physiotherapy.

Necrotic tissue or organ must be surgically removed. The exception to this rule is individual species necrosis: necrosis in which the surgical risk is higher than the risk of the outcome of the preoperative condition (for example, myocardial infarction), small infarction, encapsulated necrosis with a tendency to organize or transform into an ulcer or cyst.

In case of coagulative necrosis, dry gangrene, surgery can be postponed until the necrotic tissue is completely isolated. At the same time, it is important to prevent the development of liquefaction necrosis (wet gangrene), therefore local conservative treatment of dry necrosis is carried out with strict adherence to asepsis using drying agents: open method of treatment, exposure to warm air (24 - 25 ° C) under a metal frame with light bulbs, covered with sterile sheets, lubricating tissues with solutions of 1% brilliant green, 5% iodine, 10% potassium permanganate or silver nitrate, 5% tannin, the use of alcohol dressings, physiotherapeutic procedures (UVR, UHF, etc.). After the appearance of the demarcation line, necrotomy (dissection of necrosis), necrectomy (removal of necrosis) or amputation is performed.

Necrotomy is performed for extensive necrosis of the limb and chest, since necrosis, disrupting innervation, blood and lymph circulation, impairs the nutrition of deeper tissues (or limbs in case of circular necrosis) and makes breathing difficult. Necrotic tissue is dissected to bleeding viable tissue in several places, often without (necrotic tissue is painless).

Necrectomy (excision of dead tissue) is carried out within viable tissues after the appearance of a demarcation line or after determining the boundaries of necrosis using mechanical irritation (prick with a syringe needle, touching surgical instrument, ball, etc.). The tissue defect formed after necrectomy is closed by suturing or dermatoplasty.

Amputation of a limb or its segment is carried out forcibly for health reasons (transformation of dry gangrene into progressive wet). In case of liquefaction necrosis, wet gangrene, it is necessary to try to convert them into dry condition drying agents. The ineffectiveness of these measures and progressive wet necrosis with intoxication are indications for emergency or urgent necrectomy, amputation within viable tissues. In case of wet gangrene of internal organs, surgery is always performed as an emergency.

IN healthy body when attacked by pathogenic microorganisms, immune reactions are triggered. But in some cases, a malfunction occurs, and microbes that have penetrated into the tissue cause significant destruction. As a result of exposure to negative external and internal factors, tissue necrosis (death) begins.

Forms and types of necrosis

Experts distinguish two forms of necrosis:

1. Coagulation necrosis (dry) occurs when tissue protein folds in the absence of blood flow and as a result of intense evaporation of moisture. In this case, the affected areas acquire a yellow-gray or dark brown tint. The tissues become dry and brittle, suppuration occurs, an abscess is formed, and when it opens, a fistula occurs.
2. Liquation necrosis (wet) is characterized by swelling and liquefaction of dead tissue. As a result of necrosis, a gray mess with a pronounced putrefactive odor is formed.

There are several types of necrosis:

• necrosis muscle tissue(waxy or Zenker's) is associated with damage to skeletal muscles;
• adipose tissue necrosis – irreversible processes in adipose tissue;
• connective tissue necrosis;
• caseous necrosis, manifested in the fact that the affected areas begin to crumble;
• gangrene – necrosis of soft tissues (upper and lower extremities) and internal organs;
• sequester – necrosis of hard (bone) tissue;
• a heart attack that occurs as a result of circulatory disorders in individual organs or tissues.

Symptoms of tissue necrosis

One of the first symptoms of necrosis is loss of sensation and numbness. In this case, the skin in the affected area looks noticeably paler than the adjacent healthy tissue and takes on a characteristic “waxy” appearance. Therapy started in the initial period of the disease helps stop pathological changes. At this stage, it is still possible to restore blood circulation. If measures have not been taken, the skin becomes bluish in color, after which it quickly turns black. Other signs of soft tissue necrosis of the extremities are:

• convulsions;
• trophic ulcers.

Regardless of the area affected by necrosis, disturbances occur in the following activities:

• nervous system;
• kidney;
• liver;
• respiratory system.

This is accompanied by:

• decreased immunity;
• metabolic disorder leading to hypovitaminosis and general exhaustion;
• poor health, constant overwork.

Treatment of tissue necrosis

Therapy for dry and wet necrosis has a number of fundamental differences.

Local treatment for coagulative necrosis consists of:

1. Measures to prevent the spread of pathology, including:

• treating the skin near the affected area with antiseptics;
• applying bandages with disinfectants;
• drying the skin at the site of infection with alcoholic brilliant green or a 5% solution of potassium permanganate.

2. Necrectomy (excision of non-viable tissue).

Necrosis (from Greek nekros - dead)- necrosis, death of cells and tissues in a living organism, while their vital activity completely ceases. Changes that precede necrosis and are represented by irreversible dystrophic processes are called necrobiosis, and necrobiosis extended over time is called pathobiosis.

Tissue necrosis - causes, symptoms, diagnosis and treatment

These are the processes of slow tissue dying due to disruption of innervation, non-healing ulcers due to general exhaustion, etc.
Close to necrobiosis is the concept of paranecrosis (D.N. Nasonov, V.Ya. Aleksandrov). It includes a set of signs (increased viscosity of colloids of the cytoplasm and nucleus, changes in the electrolyte composition, increased sorption properties of the cytoplasm), reflecting reversible changes in the cell that characterize local widespread excitation. In this regard, paranecrosis is considered as a morphological expression of parabiosis.
Necrobiotic and necrotic processes occur constantly as a manifestation of the normal functioning of the body, since the performance of any function requires the expenditure of a material substrate, which is replenished by physiological regeneration. Thus, the integumentary epithelium of the skin, the epithelium of the respiratory, digestive and genitourinary tracts constantly die and regenerate. Cells also die and regenerate during holocrine secretion, macrophages during phagocytosis, etc.
In addition, it should be borne in mind that most of the body’s cells are constantly subject to aging, “natural death” and subsequent renewal, and life expectancy different cells different and determined genetically. The “natural death” of a cell, which completes its aging, is followed by physiological necrosis, i.e., cell destruction, which is based on the processes of autolysis.

Microscopic signs of necrosis. These include characteristic changes in the cell and intercellular substance. Cell changes affect both the nucleus and the cytoplasm.
The nucleus shrinks, and chromatin condenses (karyopyknosis), breaks up into clumps (karyorrhexis), 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 removal of phosphate groups from nucleotides and the release nucleic acids, which undergo depolymerization.
Denaturation and coagulation of proteins occur in the cytoplasm, usually followed by colliquation, and its ultrastructures die. The changes may involve part of the cell (focal coagulative necrosis), which is rejected, or the entire cell (coagulation of the cytoplasm). Coagulation ends with plasmorexis - the breakdown of the cytoplasm into clumps. At the final stage, the destruction of the membrane structures of the cell leads to its hydration, and 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 degeneration). Focal necrosis may occur full recovery outer membrane of the cell. 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.
Changes in the intercellular substance during necrosis cover both the interstitial substance and fibrous structures. Due to depolymerization of its glycosaminoglycans and impregnation with blood plasma proteins, the intermediate substance swells and melts. Collagen fibers also swell, become saturated with plasma proteins (fibrin), transform into dense homogeneous masses, disintegrate or lyse. Changes in elastic fibers are similar to those described above: swelling, basophilia, disintegration, melting - elastolysis. Reticular fibers often remain in foci of necrosis for a long time, but then undergo fragmentation and lumpy decay; changes in nerve fibers are similar. 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 most often develop. Less often, they manifest themselves as pronounced swelling and mucus of the tissue, which is characteristic of liquefaction necrosis. With necrosis of adipose tissue, lipolytic processes predominate. Neutral fats are broken down to form fatty acids and soaps, which leads to reactive inflammation and the formation of lipogranulomas (see 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 is formed. Demarcation inflammation develops around the focus of necrosis.
With tissue necrosis, their consistency, color, and smell change. In some cases, dead tissue becomes dense and dry (mummification), in others it becomes flabby and melts (myomalacia, encephalomalacia from the 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 is the foci of circulatory necrosis in the lungs that arise against the background of venous stagnation. Foci of necrosis of the skin, intestines, and uterus often acquire a dirty brown, gray-green or black color, as the substances that impregnate them blood pigments undergoing a number of changes. In some cases, foci of necrosis are stained with bile. When putrefactively melts, dead tissue emits a characteristic foul odor.

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Types of necrosis

Topic: “Necrosis. Ulcers. Fistulas. Causes, diagnosis and treatment principles.

Work organization nurse».

Lesson plan.

1. Reasons for the development of necrosis.

2. Main types of necrosis.

3. Dry and wet gangrene, clinical signs, diagnosis, principles of treatment, prevention.

4. Bedsores, clinical signs, diagnosis, principles of treatment, prevention.

5. Trophic ulcers, clinical signs, diagnosis, principles of treatment, prevention.

6. Fistulas. Clinical signs, diagnosis, principles of treatment, prevention.

7. Features of organizing the work of a nurse during the development of necrosis.

Necrosis, or necrosis, is the death of cells, tissues or organs that occurs in a living organism. The cause of death may be direct destruction by a traumatic factor or circulatory disorder.

The most common causes of local tissue necrosis are: factors:

1) mechanical(compression, crushing, ruptures);

2) thermal(exposure to temperature factors above +60°C or below -10°C);

3) electric(at the place of influence electric current high voltage creates a very high temperature);

4) chemical(acids, coagulating cell proteins, cause dry coagulation necrosis, and alkalis, dissolving proteins, cause wet coagulation necrosis);

5) toxic(the effect of waste products or decay of microorganisms);

6) neurogenic(trophic tissue disorders as a result of damage to the nerve trunks of the spinal cord);

7) circulatory(cessation of blood supply to an area of ​​the body or organ as a result of prolonged spasm or obliteration of a vessel, blockage of a vessel by a thrombus or compression of the vessel with a tourniquet, tumor).

Types of necrosis

The following types of necrosis are distinguished: infarction; sequestration; coagulation (dry) necrosis; liquefaction necrosis; gangrene.

Heart attack (from Latin infarcire - stuff, stuff) - a focus of tissue or organ that has undergone necrosis as a result of a sudden cessation of its blood supply, i.e. ischemia. Therefore, infarction is also called ischemic necrosis. This term is more often used to refer to necrosis of a part of an internal organ: infarction of the brain, heart (myocardium), lung, intestines, kidney, spleen, etc.

A small infarction undergoes autolytic melting (resorption) followed by complete tissue regeneration. Most often, a heart attack develops as a type of coagulation necrosis, less often - a liquefaction one. Unfavorable outcomes of a heart attack are disruption of the vital functions of a tissue or organ, developing complications, sometimes ending in death.

Sequestration (from Latin sequestratio - separation, isolation) - a necrotic area of ​​tissue or organ located in a sequestral cavity filled with pus and separated from viable tissues by a demarcation line.

Magazine headings

The demarcation line consists of a shaft of leukocytes and an area of ​​granulation and connective tissue. More often, sequestration is formed in the bone during osteomyelitis, less often in soft tissues. It does not undergo autolysis and organization, but is melted by proteolytic enzymes of leukocytes or removed from the sequestral cavity through fistulous tracts.

Coagulation (dry) necrosis - necrosis, developing on the basis of protein coagulation and tissue dehydration. The latter become atrophic, dry (mummified), wrinkled, dense, differently colored (mainly in dark color) and delimited from viable tissues by a demarcation line, above which the necrotic process does not extend. General symptoms are mild. This type of necrosis predominantly occurs in tissues rich in proteins and poor in fluids, and is observed in chronic arterial insufficiency and aseptic conditions. Dry necrosis is poorly susceptible to hydrolytic cleavage. It can be torn away on its own, encapsulated and organized, i.e. undergo scarring, calcification (petrification), ossification (transformation into bone tissue), or melt (dissolve) as a result of autolysis with the formation of an ulcer or cavity - a cyst.

Unfavorable outcomes of dry necrosis are its transformation into liquefaction necrosis with purulent-putrefactive infection and disruption of the vital functions of tissues and organs, developing complications, sometimes ending in death.

Liquation (wet) necrosis - necrosis, characterized by melting by putrefactive microorganisms
incapable tissues. The latter become painful, swollen, tense, loose, soft, differently colored (first pale, marbled, yellowish, then cyanotic red, finally dirty and black, gray-green) with the presence of dark-colored lesions , blisters of exfoliated epidermis (phlyctenas) with ichor fluid, fetid, putrid odor. Violation of tissue integrity, decaying tissues are favorable factors for seeding and development of secondary pathogenic microflora. The necrotic process is not prone to delimitation, but, on the contrary, quickly spreads to the surrounding viable tissue. Expressed general symptoms intoxication.

Liquation necrosis can sometimes separate and transform into coagulation necrosis or melt (dissolve) to form an ulcer or cyst cavity. As a rule, wet necrosis without its elimination ends in death from disruption of the vital functions of tissues, organs, and systems as a result of progressive intoxication.

Gangrene (Greek gangraina - fire) - necrosis of tissues and organs in contact with the external environment. Distinguish gas gangrene, caused by anaerobic clostridial spore-forming microorganisms, and gangrene, which is based on coagulation necrosis - dry gangrene or liquefaction necrosis - wet gangrene. These terms are more often used for necrosis of the extremities. It is possible to develop wet gangrene of the tissues of the cheek and perineum - noma (Greek nome - “water cancer”). Gangrene of internal organs (stomach, intestines, liver, gall bladder, pancreas, kidney, bladder, lung, etc.) is always wet. A type of gangrene is bedsores.

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

Causes of necrosis

Most often, the development of necrosis results from:

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

Classification

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

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

Classification according to clinical manifestations:

1. Liquation necrosis (necrotic tissue changes accompanied by edema).
2. Coagulative necrosis (complete dehydration of dead tissue). This group includes the following types of necrosis:
3. caseous necrosis;
4. Zenker's necrosis;
5. fibrinoid necrosis of connective tissue;
6. fat necrosis.
7. Gangrene.
8. Sequestration.
9. Heart attack.

Symptoms of the disease

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

If the lower extremities are affected, the patient may have complaints of lameness, convulsions, and trophic ulcers. Necrotic changes in internal organs lead to a deterioration in the general condition of the patient, the functioning of individual body systems (central nervous system, digestive, respiratory, etc.) is disrupted.

With liquefaction necrosis, a process of autolysis is observed in the affected area - tissue decomposition under the influence of substances released by dead cells. This process results in the formation of capsules or cysts filled with pus. The most typical picture of wet necrosis is for tissues rich in fluid. An example of liquefaction necrosis is ischemic cerebral stroke. Diseases accompanied by immunodeficiency (cancer, diabetes) are considered predisposing factors to the development of the disease.

Coagulative necrosis, as a rule, occurs in tissues that are poor in fluid but contain a significant amount of protein (liver, adrenal glands, etc.). The affected tissues gradually dry out, decreasing in volume.

• With tuberculosis, syphilis, and some other infectious diseases, necrotic processes are characteristic of internal organs, and the affected parts begin to crumble (caseous necrosis).
• With Zenker's necrosis, the skeletal muscles of the abdomen or thighs are affected; the pathological process is usually triggered by pathogens of typhoid or typhus.
• At fat necrosis irreversible changes in fatty tissue occur as a result of injury or exposure to enzymes from 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 a mandatory connection, direct or indirect, with the external environment. Therefore, gangrenous necrosis affects only those organs that have access to air through anatomical channels. The black color of dead tissue is due to the formation of the chemical compound iron hemoglobin and environmental hydrogen sulfide.

What is oral tissue necrosis?

There are several types of gangrene:

• Dry gangrene is the mummification of affected tissues, most often developing in the extremities due to frostbite, burns, trophic disorders due to diabetes mellitus or atherosclerosis.
• Wet gangrene usually affects internal organs when the affected tissues become infected and has signs of liquefaction necrosis.
• Gas gangrene occurs when necrotic tissue is damaged by anaerobic microorganisms. The process is accompanied by the release of gas bubbles, which is felt when palpating the affected area (a symptom of crepitus).

Sequestrum most often develops with osteomyelitis; it 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 tissue in this pathology is gradually replaced by connective tissue, forming a scar.

Outcome of the disease

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

Diagnostics

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

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

Using these methods, it is possible to determine the exact location and size of the affected area, identify characteristic changes in tissue structure to establish accurate diagnosis, forms and stages of the disease.

Superficial necrosis, for example, gangrene of the lower extremities, does not present difficulties for diagnosis. The development of this form of the disease can be assumed based on the patient’s complaints, the bluish or black color of the affected area of ​​the body, and lack of sensitivity.

Treatment of necrosis

In case of necrotic tissue changes, hospitalization in a hospital for further treatment is required. For a successful outcome of the disease, it is necessary to correctly determine its cause and timely take measures to eliminate it.

In most cases it is prescribed drug therapy, aimed at restoring blood flow to the affected tissues or organ; if necessary, antibiotics are administered and detoxification therapy is carried out. Sometimes the only way to help a patient is surgically, by amputating part of the limbs or excision of dead tissue.

In case of skin necrosis, traditional medicine can be used quite successfully. In this case, baths made from a decoction of chestnut fruits, an ointment made from lard, slaked lime and oak bark ash are effective.

At histological examination in the collapsing tissue, characteristic changes are revealed that occur both in the cells (changes in the nucleus and cytoplasm) and in the intercellular substance.

Changes in cell nuclei. Early degenerative changes are accompanied by a decrease in the size of the nucleus and its hyperchromia ( karyopyknosis). Subsequent changes depend on the mechanism of cell death.

Necrosis - what is it?

Passive cell death is accompanied by hydration of the nucleoplasm and an increase in the nucleus, which in histological preparations appears light due to edema ( core swelling). With apoptosis, on the contrary, there is an increase in karyopyknosis. Changes in the cell nucleus during necrosis culminate in its disintegration, fragmentation ( karyorrhexis). Complete destruction of the core is denoted by the term karyolysis (carylysis).

Changes in the cytoplasm. Changes in the cytoplasm depend on the form of cell death. Apoptosis is accompanied by compaction of the cytoplasm due to dehydration of the matrix ( coagulation of the cytoplasm), the cytoplasm is stained more intensely, and its volume decreases. With passive cell death, on the contrary, progressive edema (hydration) of the hyaloplasm and organelle matrix develops. Hydration of the cytoplasmic structures of parenchymal cells in pathology is designated by the term hydropic dystrophy, and pronounced swelling of organelles (endoplasmic reticulum, mitochondria, elements of the Golgi complex, etc.) is called « balloon dystrophy» , or "focal liquefaction cell necrosis". Fragmentation (“lumpy disintegration”) of the cytoplasm is usually designated by the term plasmorrhexis However, plasmorrhexis develops fully only during apoptosis (the phase of formation of apoptotic bodies). The destruction of the cytoplasm is called plasmolysis (plasmalysis).

Changes in intercellular structures. During necrosis, the structures of the extracellular matrix (ground substance and fibers) are also destroyed. Proteoglycans (the main substance of fibrous connective tissue) depolymerize most quickly, while reticular (reticulin) fibers take the longest to destroy. Collagen fibers first increase in size due to edema, then become defibrated (divided into thinner threads) and destroyed ( collagenolysis). Elastic fibers break up into separate fragments ( elastorhexis), after which they are destroyed ( elastolysis).

DEMARCATED INFLAMMATION. OUTCOMES OF NECROSIS

Detritus is removed from the body (resorbed) during the so-called demarcation inflammation with the participation of neutrophilic granulocytes and macrophages (histiocytes). Demarcation inflammation– inflammation developing around the focus of necrosis. Demarcation inflammation, like inflammation in general, ensures the creation of conditions for restoring the integrity of damaged tissue. The main microscopic signs of inflammation are vascular congestion ( inflammatory hyperemia), swelling of perivascular tissue ( inflammatory edema) and the formation in it cellular inflammatory infiltrate. Granulocytes and monocytes migrate from the lumen of full-blooded vessels to the site of tissue damage. Neutrophil granulocytes, thanks to their lysosomal enzymes and active oxygen metabolites, melt detritus and contribute to its liquefaction. The detritus prepared in this way is then phagocytosed by macrophages ( histiocytes), formed from blood monocytes or migrating here from nearby areas of fibrous connective tissue.

After removal (resorption) of detritus, restoration occurs ( repair) damaged tissue. As a rule, small foci of destruction with an adequate course of demarcation inflammation are restored completely ( full reparation – restitution), i.e. In place of the damaged tissue, tissue similar to it is regenerated. In case of large volumes of tissue damage, as well as in case of certain violations of demarcation inflammation, the focus of necrosis is replaced scar tissue(dense, unformed, low-vascular fibrous tissue). This tissue repair is called incomplete reparation, or substitution, and the process of replacing detritus with fibrous connective tissue is organization. Scar tissue may be subject to degenerative changes – hyalinosis And petrification(see below). Sometimes bone tissue forms in the scar ( ossification). In addition, at the site of necrosis, for example, in brain tissue, a cavity (cyst) may form.

The course of demarcation inflammation may be disrupted. Its most vulnerable link is the function of neutrophil granulocytes. There are two main types pathology of demarcation inflammation: insufficient and increased activity of neutrophil granulocytes at the site of damage.

1. Insufficient activity neutrophilic granulocytes in the area of ​​necrosis, as a rule, is associated with the presence of factors that prevent chemotaxis (directed movement of these cells to the site of damage). In this case, part of the detritus, sometimes significant, remains in the tissue, becomes sharply compacted due to dehydration and is surrounded by scar tissue, forming a capsule around the necrotic masses. Thus, Mycobacterium tuberculosis usually inhibits the migration of neutrophilic granulocytes, therefore, in foci of tuberculosis lesions, caseous detritus is resorbed slowly and remains for a long time (persists).

2. Increased activity neutrophilic granulocytes occurs when detritus is contaminated with microorganisms, primarily pyogenic bacteria. Developing in the focus of necrosis purulent inflammation may spread to adjacent healthy tissue.

Thus, we can distinguish favorable(complete resorption of detritus followed by restitution of damaged tissue), relatively favorable(persistence of detritus, its organization, petrification, ossification, cyst formation at the site of necrosis) and unfavorable(purulent melting) outcomes of necrosis.

Necrosis is the death of tissue or an entire organ. In the presence of this state complete or partial violation metabolism, which sooner or later becomes the cause of their complete incapacity. Development of this pathological condition occurs in four stages. During the first stage, reversible changes are observed, called in medicine paranecrosis. In the second stage, irreversible dystrophic changes appear on the face, which are also called necrobiosis. The third stage of development of this disease is accompanied by autolysis, that is, the decomposition of the dead substrate. And finally, at the fourth stage of development of this pathology, complete cell death occurs. It is difficult to predict how long all these stages will take, since this disease is very unpredictable.

As for the reasons for the development of this pathology, there are not just many of them, but a lot. First of all, these are numerous mechanical injuries.

Necrosis - description of the disease

In addition, burns and frostbite can provoke the development of necrosis. Ionized radiation is another fairly common cause of this condition. Quite often, this type of damage occurs as a result of exposure to chemical factors such as acid and alkali. Infectious and non-infectious diseases such as diabetes mellitus and tuberculosis can also trigger the development of necrosis. It can make itself felt against the background of certain disorders of the nervous or vascular trophism of tissue.

We also draw the attention of all readers to the fact that this type of tissue death in most cases is observed in quite important organs human body. Most often the heart, brain and kidneys are affected. Try to comply healthy image life in order to prevent the development of this disease. Before use, you should consult a specialist.

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