Dry necrosis of skin tissue treatment. Soft tissue necrosis: treatment, symptoms. Treatment of necrosis in official medicine

CHAPTER 13 NECROSES (DERTIFICATIONS)

In a healthy human body, cell death and regeneration constantly occur: cells of the epidermis and epithelium of the upper respiratory tract are exfoliated, blood cells are destroyed, and their place is taken by newly formed cells, while the functions of the organs are not affected.

Such processes are normal for the body and contribute to its constant renewal. However, necrosis of tissues, and sometimes even entire organs, can be pathological in nature and significantly impair the function of organs and systems.

Necrosis is the death of tissues, entire organs or parts thereof in a living organism.

The reasons for the development of necrosis may be different. According to etiology, all necrosis is divided into two large groups: direct and indirect.

Direct necrosisarise directly in the area of influence of any external factor. Cell death can be caused by mechanical force and is expressed to varying degrees in both closed (fractures, dislocations, ruptures, etc.) and open (wounds) injuries.

Necrosis can occur in burns under the influence of a physical (high temperature, electric current, radiation energy) or chemical (acid or alkali) factor on the body. The death of cells and tissues of the body due to the activity of pathogenic microorganisms is one of the components of purulent diseases and complications.

Direct necrosis that develops under the influence of the listed factors is very peculiar and is discussed in detail in the relevant chapters of the textbook.

This chapter focuses on consideration of issues of etiology and pathogenesis, clinical picture and treatment indirect necrosis. Considering the leading importance in the development of indirect necrosis of the vascular factor, they are otherwise called circulatory.

Etiology and pathogenesis of circulatory necrosis

The occurrence of circulatory (indirect) necrosis is associated with disruption of the nutrition of cells and tissues in a living organism. For their development

tia does not require direct external influence on a certain area of the body; necrosis occurs as if by itself, due to internal reasons.

Classification

The main reasons for the development of circulatory necrosis:

Impaired arterial patency;

Violation venous outflow;

Violation of microcirculation;

Impaired lymph circulation;

Violation of innervation.

These causes may occur acutely or gradually due to progression chronic diseases.

In some cases, necrosis also develops due to disturbances in systemic hemodynamics. The development of trophic ulcers (one of the types of necrosis) on the legs with arterial hypertension has been described.

Acute and chronic arterial obstruction

Impairment of arterial blood flow is the most common reason development of circulatory necrosis, since the lack of oxygen supply to the tissues and nutrients causes cell death quite quickly. Arterial obstruction may occur acutely and develop gradually.

Acute arterial obstruction

Acute disruption of arterial blood supply is most dangerous due to the development of massive tissue necrosis. In this case, severe, difficult-to-control pain in the limb occurs; the skin acquires a marbled color (pale with bluish spots) and becomes cold; ischemic muscle contracture often occurs, sensory disturbance, paresthesia. Patients are forced to lower the limb down, which, due to a slight increase in blood flow, helps reduce pain.

The most well-known classification of the stages of acute ischemia proposed by V.S. Savelyev.

Stage of functional impairment continues for several hours. Characterized by sharp pain, pallor and coldness of the extremities.

you. There are no sensory disorders or pronounced limitation of movements. When blood flow is restored, the function is completely normalized.

Stage of organic change. The duration of ischemia is up to 12-24 hours. The described picture is accompanied by disturbances in tactile and pain sensitivity and limitation of movements due to muscle contracture. Restoring blood flow allows the limb to be saved, but there is limited function.

Necrotic stage usually occurs within 24-48 hours. A picture of necrosis of the limb develops, starting from its most distal parts (from the tips of the fingers, from the foot). Restoring blood flow in some cases only reduces the developing zone of necrosis.

In stages 1 and 2, it is necessary to restore blood flow, which will help eliminate ischemia and reverse the development of symptoms. At the 3rd stage, irreversible changes occur and the patient’s life is threatened, therefore the main methods of treatment are necrectomy and amputation.

The degree of developing ischemia in acute disturbance of arterial blood flow is largely related to the development of collaterals in the patient in this area.

In diagnostic terms, determining the pulsation of peripheral arteries is extremely important. Its absence at a certain level allows us to establish a topical diagnosis of vessel damage.

To confirm the diagnosis and clarify the nature, localization and extent of vessel damage, special research methods are used: rheovasography, Dopplerography and angiography.

The main causes of acute arterial circulatory disorders:

Damage main vessel;

Thrombosis;

Embolism.

Damage to the great vessel

In case of injury, an artery may be crossed, compressed by bone fragments, and a pulsating hematoma may form, compressing the main vessel. In this case, the pulsation of the artery distal to the damage zone ceases to be detected and a characteristic clinical picture of acute ischemia develops. It should be noted that with any injury there is a pronounced pain syndrome and changes in skin color in the damaged area, which can make it difficult to diagnose circulatory disorders. In this regard, it is necessary to determine the peripheral pulsation

ric arteries when examining a trauma victim, and, if necessary, the use of special diagnostic methods.

Traumatic injuries to the arteries can conditionally include the application of a tourniquet to a limb for a long period of time, as well as accidental intraoperative ligation of the artery. For example, when removing the gallbladder, instead of the cystic artery, an abnormally located hepatic artery can be ligated, which can cause the development of necrosis in the liver and lead to the death of the patient.

The main methods of restoring blood flow through a damaged main artery are applying a vascular suture, prosthetics or bypass surgery of the damaged vessel.

Thrombosis

Closure of a main artery by a thrombus usually occurs against the background of previous damage to the vascular wall due to chronic vascular disease, as well as with an increase in blood viscosity and coagulability.

The clinical picture is dominated by classic symptoms of acute ischemia. It should be noted that in some cases they are moderately expressed; the symptoms are smoothed out. This is explained by the fact that as a result of previous chronic damage to the main artery, collaterals developed quite actively. The severity of clinical manifestations and the nature of necrosis depend on the level of thrombosis and its extent.

Restoration of blood flow during thrombosis is carried out by intimothrombectomy or bypass. The earlier the operation is performed, the less likely the development and extent of necrosis.

Embolism

Embolism is a blockage of a vessel brought by a blood clot, less often by air or fat.

Depending on the location of the embolus, embolism is distinguished pulmonary artery and embolism of arteries of the systemic circulation (carotid, femoral, mesenteric, etc.).

The causes of pulmonary embolism are thrombophlebitis of the veins of the systemic circulation, most often the veins lower limbs and small pelvis.

Thromboembolism of the arteries of the systemic circulation occurs in heart diseases (septic endocarditis, mitral stenosis).

valve, atrial fibrillation etc.), as well as in atherosclerosis of the aorta and its branches.

An air embolism is a consequence of a violation of the rules of infusion therapy, when air enters the patient’s vessels. Its occurrence is also possible when the veins of the neck are damaged (they collapse poorly, and air can enter them when inhaling under negative pressure).

There are typical sites of thromboembolism. The embolus almost always gets stuck at the site of bifurcation or narrowing of the vessel. Typical localizations of an embolus in the brachial artery: the space between the scalene muscles, the origin of the deep brachial artery, the site of division into the radial and ulnar artery; in the vessels of the lower extremities - bifurcation abdominal aorta, at the site of division of the iliac artery into external and internal, at the site of origin of the deep femoral artery, at the exit of the femoral artery from the muscular space of the abductor muscles, at the site of division into the anterior and posterior tibial arteries.

The clinical picture of thromboembolism consists of the sudden appearance of symptoms of acute ischemia. The severity of symptoms, as well as the frequency of development of extensive necrosis, is greater than with thrombosis. This is due to the fact that in most cases, emboli block unchanged main arteries, leading to an immediate cessation of powerful normal blood flow, and collaterals are usually not yet developed.

The method of treatment is embolectomy (except for extreme ischemia), and in case of previous vascular damage, reconstructive surgery.

There are direct and indirect embolectomy.

At straight embolectomy, an incision is made in the area where the embolus is located, the artery is opened, the embolus is mechanically removed and a vascular suture is applied. Currently, direct embolectomy has given way to indirect (Fogerty's operation).

Advantages indirect embolectomy:

There is no need to know exactly the location of the embolus;

The operation is performed from the most convenient places for access (both in the proximal and distal directions);

The artery is dissected in the intact zone, which reduces the risk of thrombosis.

To perform indirect embolectomy, a Fogarty catheter is used - a catheter with a special rubber balloon at the end.

After a typical access to the corresponding main artery is made, the latter is opened and a Fogarty catheter is inserted into its lumen (Fig. 13-1).

Rice. 13-1.Indirect embolectomy with a Fogarty catheter: a - Fogarty catheter; b - removal of the embolus in the proximal and distal directions

The catheter is advanced beyond the area where the thrombus is located, the balloon is inflated using a syringe with an inert solution and the catheter is pulled out, removing the embolus in the artery and restoring blood flow.

Chronic arterial obstruction

A gradual decrease in the diameter of the artery (stenosis) up to complete blockage develops in so-called obliterating diseases. The most common among them obliterating atherosclerosis And obliterating endarteritis.

Obliterating diseases affect various main vessels (carotid, coronary, mesenteric, renal arteries), but in surgery, damage to the vessels of the lower extremities is of particular importance, most often causing the development of necrosis.

Clinical picture

The main symptom in the clinical picture of obliterating diseases with the development of chronic limb ischemia is the symptom intermittent claudication: when walking there is severe pain in the calf muscles, which forces the patient to stop, while the pain subsides and he can walk again, then the situation repeats.

The severity of the symptom of intermittent claudication indicates the depth of the disturbance in the blood supply to the extremities and determines the degree of chronic ischemia:

I degree - pain occurs after 500 m of walking;

II degree - after 200 m of walking;

III degree - after walking less than 50 m and at rest;

IV degree - the appearance of foci of necrosis.

Patient complaints of cold feet and legs and paresthesia are typical.

The most important predisposing factor for the development of obliterating diseases of the vessels of the lower extremities is smoking (!).

An objective examination reveals limb hypotrophy; hair loss; the limb is pale and cold to the touch. With IV degree of ischemia, necrosis occurs (trophic ulcers, gangrene). Localization of necrosis on the fingers (especially on the distal phalanges) and in the heel area is typical. This is due to the greatest distance of these zones from the heart, which creates the worst conditions for blood supply.

For topical diagnosis of vascular lesions, it is necessary to determine the pulsation of the great vessels, conduct Dopplerography and angiography.

Clinical differences between obliterating atherosclerosis and endarteritis

Despite the fact that both obliterating atherosclerosis and obliterating endarteritis cause the development of chronic limb ischemia, they have a number of significant differences. The main features of the clinical course of the diseases are presented in Table. 13-1.

Table 13.1.Clinical differences between obliterating atherosclerosis and obliterating endarteritis

Treatment methods chronic disorder Arterial patency is divided into conservative and surgical.

Conservative treatment

Conduct complex treatment. Taking into account the characteristics of the disease, indications and contraindications, the following drugs and methods are used:

Antispasmodics (drotaverine, nicotinic acid);

Anticoagulants (sodium heparin, phenindione);

Angioprotectors (pentoxifylline);

Prostaglandin E preparations (alprostadil);

Drugs that increase tissue resistance to hypoxia;

Physiotherapeutic effects on the lumbar sympathetic ganglia.

Surgery

Lumbar sympathectomy interrupts sympathetic innervation, reducing spastic contraction of the vessels of the lower extremities, and promotes the opening of collaterals. Improved blood flow

non-radical, which makes the method close to conservative treatment diseases.

Intimothrombectomy (endarterectomy) - removal of an atherosclerotic plaque with thrombotic masses along with the intima of the vessel. Used for local narrowing of the vessel due to a pathological process. There are open and semi-closed intimothrombectomy (Fig. 13-2).

Rice. 13-2.Intimothrobectomy according to Dos Santos: a - open; b - semi-closed (using a loop and a disobliterotome)

Prosthetics and shunting. The affected area of the vessel is replaced with a prosthesis (prosthetics) or above and below the site of stenosis in the vessel

Rice. 13-3.Femoropopliteal bypass with autovenous vein

Rice. 13-4.Aortofemoral bifurcation bypass with a synthetic prosthesis

a shunt is sewn in, creating conditions for a roundabout flow of blood (shunting). The autovein (great saphenous vein of the patient’s thigh) or synthetic dentures from lavsan, velor, etc. (Fig. 13-3 and 13-4). In some cases, an allograft from the umbilical cord vessels is used. To bypass vessels of medium and small caliber, the “bypass in situ” bypass technique is used (instead of the affected artery, blood flow is “allowed” through the vein located here in the opposite direction using proximal and distal anastomoses with the corresponding arteries, having previously destroyed the vein valves with a special stripper).

Methods of endovascular surgery are based on the introduction of special catheters and instruments into the lumen of the artery, which make it possible, under X-ray control, to dilate the stenotic section of the artery (using a special catheter with a balloon at the end), laser recanalization (the atherosclerotic plaque is “burned out” with a laser beam), and installation of a peculiar vessel frame (stent).

Violation of venous outflow

Disruption of venous outflow, as well as the influx of arterial blood, worsens the living conditions of cells and tissues, but the consequences of these disturbances are somewhat unique.

Differences in necrosis in violation

venous outflow and arterial blood supply

In case of venous outflow disturbance clinical manifestations onset more slowly, swelling and cyanosis prevail skin. In the absence of inflammation, the pain syndrome is moderate. Bo-

The development of small superficial necrosis (trophic ulcers) is more typical, while when the arterial blood supply is disrupted, extensive necrosis and gangrene of the extremities often occur (trophic ulcers are also possible). With venous pathology, the development of gangrene without the addition of infection does not occur.

At the same time, when the venous outflow is disrupted, pronounced trophic disorders of the skin and subcutaneous tissue occur: tissue compaction (induration) is characteristic, and they acquire a brown color (pigmentation).

Localization of necrosis is characteristic. In arterial insufficiency, tissue necrosis usually begins from the fingertips and heel area, that is, in the places most distant from the heart. At venous insufficiency Due to the structural features of the venous bed of the lower extremities, the worst conditions for tissues are created in the area of the medial ankle and in the lower third of the leg, where trophic ulcers usually form.

Violations of venous outflow can be acute or chronic.

Acute violation of venous outflow

Acute disruption of venous outflow can be caused by acute thrombophlebitis, thrombosis and damage to the main veins.

For the development of necrosis, damage to the deep veins of the lower extremities is important. Damage to the superficial veins is dangerous only as a source of thromboembolism.

Clinical picture

Acute deep vein thrombosis is manifested by the sudden appearance of moderate aching pain in the limb, aggravated by movement, as well as progressive swelling and cyanosis of the skin. The superficial veins are clearly contoured and bulge. On palpation, sharp pain occurs along the neurovascular bundle.

Similar symptoms, with the exception of pain and soreness, occur when the deep veins are damaged (compressed). An obvious clinical picture usually does not require the use of special diagnostic methods. The diagnosis can be confirmed using a Doppler study.

In acute disorders of venous outflow, necrosis usually appears in the long-term period and is represented by trophic ulcers. Extensive necrosis in acute period are rare.

Treatment

Acute disturbance of venous outflow is treated conservatively using the following drugs:

Antiplatelet agents ( acetylsalicylic acid, dipyridamole, pentoxifylline);

Anticoagulants (heparin sodium, enoxaparin sodium, phenindione);

Methods and preparations for improving the rheological properties of blood (UVR and laser irradiation of autologous blood, dextran [molecular weight 30,000-40,000]);

Anti-inflammatory drugs (diclofenac, ketoprofen, naproxen, etc.);

Indications for surgical intervention arise for thrombophlebitis of the superficial veins in the following cases:

Ascending thrombophlebitis with the risk of the process transferring to deep veins and the development of thromboembolism - ligation and intersection of the vein is performed proximally;

Abscess formation - abscesses are opened or thrombosed veins are excised along with the surrounding tissue.

Chronic venous outflow disorder

Among chronic venous diseases, two are of primary importance in the development of necrosis: varicose and postthrombotic diseases of the lower extremities.

Varicose veins

Clinical picture. The most typical manifestation is varicose veins saphenous veins: the saphenous veins in the vertical position of the patient bulge, are tense, and have a tortuous character. Patients complain of a cosmetic defect, as well as a feeling of heaviness in the limbs towards the end of the day, and cramps at night. The disease usually progresses slowly. Slowing blood flow in dilated veins contributes to the development of trophic disorders. Edema, cyanosis, tissue induration and skin pigmentation gradually appear.

Trophic disorders are most pronounced in the lower third of the leg, in the area of the medial malleolus, where subsequently a focus of necrosis appears - a trophic ulcer.

To determine treatment tactics, special tests are used (marching, double-bandage tests, etc.), as well as additional methods.

Types of research (rheovasography, Dopplerography, X-ray contrast venography).

Surgery. Phlebectomy is performed - removal of varicose veins, in which the main trunk of the great saphenous vein is usually removed, and incompetent communicating veins are ligated. If the valves of the deep veins are incompetent, their extravasal correction is carried out using special coils.

Sclerosing therapy. Special substances (lauromacrogol 400) are injected into varicose veins, causing thrombosis and a sclerosing process with complete obliteration of the vein.

Conservative treatment does not cure the disease, but prevents its progression. Basic methods: wearing elastic bandages, using angioprotectors and venotonics (diosmin + hesperidin, troxerutin).

Postthrombotic disease

Clinical picture. Postthrombotic disease usually begins with acute deep vein thrombosis. As a result of this process, the outflow through the deep veins is disrupted, which is accompanied by swelling of the limb, a feeling of heaviness in it, and cyanosis. Trophic disorders gradually appear and progress: induration and pigmentation of the skin in the lower third of the leg, then trophic ulcers form. It is possible to develop secondary varicose veins of the saphenous veins, which bear the main burden of ensuring blood outflow. Subsequently, the patency of the deep veins can be restored (recanalization stage).

Obstruction of the patency of deep veins is detected clinically, as well as using Dopplerography and radiocontrast venography.

Conservative treatment - main method. Once every 5-6 months, patients undergo a course of vascular therapy:

Disaggregants (acetylsalicylic acid, dipyridamole, pentoxifylline);

Anticoagulants (phenindione);

Methods and preparations for improving the rheological properties of blood (UVR and laser irradiation of autologous blood, dextran [molecular weight 30,000-40,000]);

Angioprotectors and venotonics (diosmin + hesperidin, troxerutin).

Surgery. In case of complete blockage of the veins of the ileofemoral segment, surgical interventions are used to restore venous outflow from the limb. The most common operation is

tion Palma: on a healthy limb there is v. saphena magna, cut off in the lower third of the thigh while maintaining the mouth; the cut off distal end of the vein is carried over the pubis to the opposite side and anastomose with the deep vein of the thigh below the site of blockage. Thus, the outflow from the diseased limb along the displaced v. saphena magna carried out through the deep veins of a healthy limb.

Restoring the patency of veins by surgical recanalization (similar to recanalization of arteries) is usually not performed, which is associated with a high incidence of thrombosis, as well as the risk of damage to the thin venous wall.

Microcirculation disturbance

Impaired microcirculation can also lead to the development of necrosis. The main diseases in which microcirculation disorders occur: diabetes(diabetic foot), systemic vasculitis, bedsores.

Diabetic foot

In diabetes mellitus, angiopathy gradually develops, expressed mainly in arteriolosclerosis. The defeat is systemic. The vessels of the retina, kidneys, etc. are affected, but for the development of necrosis, damage to the vessels of the lower extremities, in particular the feet, is of primary importance. In this case, along with angiopathy, diabetic polyneuropathy develops, leading to a decrease in sensitivity, impaired immune status with a decrease in resistance to infection and a slowdown in reparative processes.

The listed changes in the complex received the special name “diabetic foot”. A feature of the diabetic foot is a combination of infectious onset and inflammation with microcirculatory necrosis, decreased immune and reparative processes.

It is very difficult to treat such patients. Active surgical tactics are required (necrectomy, opening of purulent leaks), antibacterial therapy, correction of blood glucose concentrations and microcirculatory disorders.

Systemic vasculitis

Systemic vasculitis is a heterogeneous group of diseases in which pathological process, characterized by inflammation

weakening and necrosis of the vascular wall, leading to ischemic changes in organs and tissues.

Vasculitis includes periarteritis nodosa and Henoch-Schönlein disease. Treatment of these diseases is individual, using complex regimens using hormonal drugs, cytostatics, immunomodulators and other drugs.

Bedsores

With pressure ulcers, the development of necrosis due to impaired microcirculation occurs due to prolonged compression fabrics. Diagnosis, prevention and treatment of bedsores are discussed in Chapter 9. In addition, it should be noted that bedsores develop not only when the patient remains in bed for a long time. Necrosis of the tracheal wall during prolonged intubation, necrosis of the mucous membrane of the esophagus and stomach from a nasogastric tube, necrosis of the intestinal wall during prolonged stay of drainage in abdominal cavity also commonly called pressure ulcers, given the mechanism of their development. Prevention of bedsores of this kind is early removal of drainages, use of tubes made of inert soft materials.

Lymphatic circulation disorder

The main disease in which lymph circulation is impaired is lymphedema. For lymphedema due to various etiological factors the outflow of lymph from organs (most often from the lower extremities) is disrupted. This leads to the appearance of edema, the accumulation of acidic mucopolysaccharides in the skin and subcutaneous tissue, and the development of massive fibrosis.

The final stage of lymphedema is fibroedema (elephantiasis) of the extremities. In this case, the limb is sharply increased in size due to fibrosis of the skin and subcutaneous tissue, the skin is thickened, often with many cracks and proliferation of papillae, areas of the skin hang down in the form of a kind of apron. Against this background, the formation of superficial necrosis (trophic ulcers) with abundant lymphorrhea is possible. In the early stages of lymphedema, necrosis does not form.

Disturbance of innervation

The trophic function of nerves is less important for the normal functioning of tissues than the blood supply, but at the same time, disruption of innervation can lead to the development of superficial necrosis - neurotrophic ulcers.

A feature of neurotrophic ulcers is a sharp inhibition of reparative processes. This is largely due to the fact that it is difficult to eliminate or at least reduce the influence of the etiological factor (impaired innervation).

Neurotrophic ulcers can form due to injury and disease spinal cord(spinal injury, syringomyelia), damage to peripheral nerves.

Main types of necrosis

All of the above diseases lead to the development of necrosis. But the types of necrosis themselves are different, which has a significant impact on treatment tactics.

Dry and wet necrosis

It is fundamentally important to divide all necrosis into dry and wet.

Dry (coagulative) necrosis characterized by the gradual drying of dead tissues with a decrease in their volume (mummification) and the formation of a clear demarcation line separating dead tissues from normal, viable ones. In this case, the infection does not occur, and the inflammatory reaction is practically absent. The general reaction of the body is not expressed, there are no signs of intoxication.

Wet (colliquation) necrosis characterized by the development of edema, inflammation, an increase in the organ's volume, while hyperemia is expressed around the foci of necrotic tissue, there are blisters with clear or hemorrhagic fluid, and the flow of cloudy exudate from skin defects. There is no clear boundary between the affected and intact tissues: inflammation and edema spread beyond the necrotic tissues to a considerable distance. The addition of a purulent infection is typical. With wet necrosis, severe intoxication develops (high fever, chills, tachycardia, shortness of breath, headaches, weakness, profuse sweating, changes in blood tests of an inflammatory and toxic nature), which, as the process progresses, can lead to dysfunction of organs and death of the patient. The differences between dry and wet necrosis are presented in table. 13-2.

Thus, dry necrosis proceeds more favorably, is limited to a smaller volume of dead tissue and poses a significantly less threat to the patient’s life. In what cases does dry necrosis develop, and in what cases does wet necrosis develop?

Table 13-2.The main differences between dry and wet necrosis

Dry necrosis usually forms when the blood supply to a small, limited area of tissue is disrupted, which does not occur immediately, but gradually. More often, dry necrosis develops in patients with low nutrition, when there is practically no water-rich fatty tissue. For dry necrosis to occur, it is necessary that there are no pathogenic microorganisms in this area, so that the patient does not have concomitant diseases that significantly worsen immune responses and reparative processes.

In contrast to dry necrosis, the development of wet necrosis is promoted by:

Acute onset of the process (damage to the main vessel, thrombosis, embolism);

Ischemia of a large volume of tissue (for example, thrombosis of the femoral artery);

Expression in the affected area of tissues rich in fluid (fatty tissue, muscles);

Attachment of infection;

Concomitant diseases (immunodeficiency conditions, diabetes mellitus, foci of infection in the body, insufficiency of the circulatory system, etc.).

Gangrene

Gangrene is a certain type of necrosis, characterized by a characteristic appearance and extent of damage, in the pathogenesis of which the vascular factor is of significant importance.

Characteristic appearance fabrics - their black or gray-green color. This color change is due to the decomposition of hemoglobin upon contact with air. Therefore, gangrene can develop only in organs that have communication with the external environment, air (limbs, intestines, appendix, lungs, gall bladder, mammary gland). For this reason, there is no gangrene of the brain, liver, or pancreas. Foci of necrosis in these organs look completely different in appearance.

Table 13-3.Differences between trophic ulcers and wounds

Damage to an entire organ or most of it. It is possible to develop gangrene of a finger, foot, limb, gall bladder, lung, etc. At the same time, there cannot be gangrene of a limited part of the body, the dorsum of a finger, etc.

In the pathogenesis of necrosis, the vascular factor is of primary importance. Its influence can be felt both at the beginning of the development of necrosis (ischemic gangrene) and at a later stage (impaired blood supply and microcirculation during purulent inflammation). Like all types of necrosis, gangrene can be dry or wet.

Trophic ulcer

A trophic ulcer is a superficial defect of the integumentary tissues with possible damage to deeper tissues, which has no tendency to heal.

Trophic ulcers usually form due to chronic disorders of blood circulation and innervation. According to etiology, atherosclerotic, venous and neurotrophic ulcers are distinguished.

Considering that with a trophic ulcer, as with a wound, there is a defect in the integumentary tissues, it is important to determine their differences from each other (Table 13-3).

The wound is characterized by a short period of existence and changes in accordance with the phases of the wound process. Usually the healing process is completed in 6-8 weeks. If this does not happen, then the reparative processes slow down sharply, and starting from the second month of existence, any defect in the integumentary tissue is usually called a trophic ulcer.

A trophic ulcer is always located in the center of trophic disorders, covered with flaccid granulations, on the surface of which there is fibrin, necrotic tissue and pathogenic microflora.

Fistulas

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.

The fistula tract is usually lined with epithelium or granulations.

If the fistula tract communicates with the external environment, the fistula is called external; if it connects internal organs or cavities - internal. Fistulas can be congenital and acquired, can form independently, due to the course of a pathological process (fistulas with osteomyelitis, ligature fistulas, fistula between the gallbladder and the stomach during a long-term inflammatory process), or can be created artificially (gastrostomy for feeding in case of a burn of the esophagus, colostomy for intestinal obstruction).

The examples given show how diverse fistulas can be. Their features, methods of diagnosis and treatment are related to the study of diseases of the corresponding organs and are the subject of private surgery.

General principles of treatment

For necrosis, local and general treatment is carried out. At the same time, there are fundamental differences in the tactics and methods of treating dry and wet necrosis.

Treatment of dry necrosis

Treatment of dry necrosis is aimed at reducing the area of dead tissue and maximizing the preservation of the organ (limb).

Local treatment

The objectives of local treatment of dry necrosis are primarily to prevent the development of infection and dry out the tissue. To do this, treat the skin around the necrosis with antiseptics and use dressings with ethyl alcohol, boric acid or chlorhexidine. It is possible to treat the necrosis zone with a 1% alcohol solution of brilliant green or a 5% solution of potassium permanganate.

After the formation of a clear demarcation line (usually after 2-3 weeks), necrectomy is performed (resection of the phalanx, amputation of a finger,

foot), and the incision line should pass in the zone of unchanged tissues, but as close as possible to the demarcation line.

General treatment

For dry necrosis, general treatment is primarily etiotropic in nature, it is aimed at the underlying disease that caused the development of necrosis. This treatment makes it possible to limit the area of necrosis to a minimum volume of tissue. Maximum efforts should be made effective measures. If it is possible to restore blood supply by intimothrombectomy or bypass surgery, this should be done. In addition, conservative therapy is carried out aimed at improving blood circulation in the affected organ (treatment of chronic arterial diseases, disorders of venous outflow and microcirculation).

Great importance for prevention infectious complications give antibiotic therapy.

Treatment of wet necrosis

Wet necrosis, accompanied by the development of infection and severe intoxication, poses an immediate threat to the patient’s life. Therefore, when they develop, more radical and vigorous treatment is necessary.

On early stage The goal of treatment is to try to convert wet necrosis to dry. If the desired result cannot be achieved or the process has gone too far, the main task becomes radical removal of the necrotic part of the organ (limb) within the obviously healthy tissue (high amputation).

Treatment in the early stages Local treatment

To transform wet necrosis into dry necrosis, local wound rinsing with antiseptics (3% hydrogen peroxide solution), opening of leaks and pockets, draining them, and dressings with antiseptic solutions (boric acid, chlorhexidine, nitrofural) are used. Immobilization of the affected limb is mandatory. The skin is treated with antiseptics with a tanning effect (96% alcohol, brilliant green).

General treatment

IN general treatment The main thing is to carry out powerful antibacterial therapy, including intra-arterial administration of antibiotics. Taking into account the presence of intoxication, detoxification therapy, correction of the function of organs and systems, as well as a complex of vascular therapy are carried out.

Surgery

Usually, it takes 1-2 days to try to convert wet necrosis to dry, although in each case the issue is decided individually. If, during treatment, swelling decreases, inflammation subsides, intoxication decreases, and the amount of necrotic tissue does not increase, conservative treatment can be continued. If after a few hours (or a day) it is clear that there is no effect from the treatment, inflammatory changes are progressing, necrosis is spreading, and intoxication is increasing, then the patient should be operated on, since this is the only way to save his life.

In cases where a patient is admitted to the hospital with wet gangrene of a limb, severe inflammation and severe intoxication, there is no need to try to convert wet necrosis into dry necrosis; short-term preoperative preparation should be carried out (infusion therapy for 2 hours) and the patient should be operated on according to emergency indications.

With wet necrosis surgery consists in removing necrotic tissue within the limits of obviously healthy, unchanged tissue. Unlike dry necrosis, given the greater severity inflammatory process, infection, in most cases, high amputation is performed. Thus, in case of wet necrosis of the foot, for example, when hyperemia and edema spread to the upper third of the leg (a fairly common situation), amputation should be performed on the thigh, preferably at the level of the middle third. Such high level amputation is due to the fact that pathogenic microorganisms are found in tissues even above the visible border of the inflammatory process. When amputation is performed close to the necrosis zone, the development of severe postoperative complications from the stump (progression of the infectious process, wound suppuration, development of necrosis), significantly worsening the general condition of the patient and the prognosis for his recovery. In some cases, it is necessary to repeat an even higher amputation.

Treatment of trophic ulcers

Treatment of trophic ulcers, the most common type of necrosis due to the characteristics of this pathological condition requires additional consideration.

For trophic ulcers, local and general treatment is used.

Local treatment

In the local treatment of a trophic ulcer, the surgeon faces three tasks: fighting infection, cleansing the ulcer of necrotic tissue, and closing the defect.

Fighting infection

The fight against infection is carried out by daily dressings, in which the skin around the ulcer is treated with alcohol or alcohol tincture of iodine, the ulcerative surface itself is washed with a 3% solution of hydrogen peroxide and bandages are applied with an antiseptic solution (3% boric acid solution, aqueous solution chlorhexidine, nitrofural).

Clearing necrotic tissue

To cleanse the ulcer surface from necrotic tissue during dressings, in addition to treating the ulcer surface with various antiseptics, necrectomy and proteolytic enzymes (chymotrypsin) are used. Local use of sorbents is possible. Physiotherapy (electrophoresis with enzymes, sinusoidal modulated currents, magnetic therapy, quartz treatment) successfully complements the treatment.

A peculiarity of trophic ulcers is that ointment dressings should not be used at any stage of treatment!

Closing a defect

After cleansing the ulcer surface and destroying pathogenic microflora, attempts should be made to close the wound defect. With small ulcers, this process goes away on its own; after cleansing the ulcer, the growth of granulations increases, and marginal epithelization appears. In this case, daily dressings should be continued using wet-dry dressings with antiseptics. In cases where the defect becomes small (less than 1 cm in diameter) and superficial, it is possible to switch to treating it with 1% alcohol

with a solution of brilliant green or a 5% solution of potassium permanganate, causing the formation of a scab, under which epithelialization will subsequently occur. Epithelialization is also promoted by the use of gel (iruksol).

To close the ulcer after cleansing, in some cases free skin grafting or excision of the ulcer with local tissue grafting can be used. However, these measures should be carried out after targeted action on the cause of the ulcer.

Effective for healing venous (but not atherosclerotic!) trophic ulcers compression therapy. Compression therapy for trophic ulcers refers to the application of a zinc-gelatin bandage to the limb, for which various modifications of Unna paste are used. Rp.: Zinci oxydati

Gelatinae ana 100.0

Glycerini 600.0

Aqua destil. 200.0

M.f. pasta

Method of applying a bandage. The patient is placed on the table, the lower limb is raised, after which the heated paste is applied with a brush from the base of the fingers to the upper third of the leg (including the area of the trophic ulcer). Following this, a layer of gauze bandage is applied. Then apply a layer of paste again with a brush, saturating the bandage with it. In total, 3-4 layers of dressing are applied in this way.

The bandage is not removed for 1-2 months. After its removal, almost all trophic ulcers up to 5 cm in size with a previously cleaned ulcerative surface are epithelialized.

Compression therapy significantly increases the possibility of closing ulcers, but not for a long period. The method does not allow a patient to be cured of trophic disorders, since it does not eliminate the cause of the disease.

General treatment

General treatment for trophic ulcers is primarily aimed at the cause of their development and consists of various methods of improving blood circulation. In this case, both conservative and surgical methods are used. For example, in the presence of a trophic ulcer due to varicose veins, in some cases, after cleansing the ulcer and suppressing the infection, phlebectomy is performed (removal of varicose veins).

Necrosis of the skin of soft tissues is a small list of what - urgently slows down and then eliminates Linguistics wave genetics - necrotic areas, neurotrophic ulcers, pathological development of pathogenic microorganisms, malnutrition of the skin, atrophy with critical development of necrosis and neurological manifestation on the largest organ.

Treatment of necrosis

With the advent of LCIM, it is not hopeless to treat necrosis and get rid of the diseased area non-surgically, by applying a compress and ointment against gangrene, a fresh wound or the process of cell decomposition after amputation of a part of a limb, wet, dry wounds, etc. First, this remedy stops the disease and in the second stage regenerates the affected area.

Wave genetics uses the restoration of the body surface, liquid and fatty environment. Cultivated for humans, enriched with micro-macroelements, programmed by quantum means, equivalents have been introduced to eliminate necrotic disease, pets were the first to experience the beneficial effects of the drug.

The liquid stops decomposition and is used as a compress twice a day at night and in the morning. The drug carries, recording genetic information programs functions as an intracellular transmitter levels out metabolic disorders of organs, using the method of holographic display of material structures, modulation information of the donor object to the recipient object. Theoretically differs in approach to solving necrotizing fasciitis.

Ointment for gangrene is used in combination with a liquid medium, a hydrophilic - fatty base with an antimicrobial agent of natural origin is used alternately, differs in color and composition and contains the corresponding quantum natural mechanisms inherent in a healthy state, the ointment works for the regeneration of the affected skin and cosmetic care of the face. Genetically, the product activates fibroblasts around the cell membrane, nourishes the dermis layer with oxygen, increases the synthesis of collagen and elastin, reduces the aggressive effects of free radicals, and restores energy balance.

The technology does not require drugs. In cases of tissue necrosis, we use biological materials together with cosmetologist colleagues; the products are manufactured under the Bioquant license, safe to handle, for external use.

If you suspect ischemia, visit your doctor. The problem remains, the verdict is amputation - if you don’t agree with this proposal, then a window of opportunity appears to solve the problem of how to save body parts using a liquid information matrix, using P.P.’s method. Garyaeva.

Disturbance of innervation

Neurotrophic ulcers can form due to damage and diseases of the spinal cord (spinal injury, syringomyelia), damage to peripheral nerves.

Main types of necrosis

All of the above diseases lead to the development of necrosis. But the types of necrosis themselves are different, which has a significant impact on treatment tactics.

It is fundamentally important to divide all necrosis into dry and wet.

Table 13-2. The main differences between dry and wet necrosis

In contrast to dry necrosis, the development of wet necrosis is promoted by:

Acute onset of the process (damage to the main vessel, thrombosis, embolism);

Ischemia of a large volume of tissue (for example, thrombosis of the femoral artery);

Expression in the affected area of tissues rich in fluid (fatty tissue, muscles);

Attachment of infection;

Concomitant diseases (immunodeficiency conditions, diabetes mellitus, foci of infection in the body, insufficiency of the circulatory system, etc.).

Considering that with a trophic ulcer, as with a wound, there is a defect in the integumentary tissues, it is important to determine their differences from each other (Table 13-3).

A trophic ulcer is always located in the center of trophic disorders, covered with flaccid granulations, on the surface of which there is fibrin, necrotic tissue and pathogenic microflora.

Fistulas

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.

The fistula tract is usually lined with epithelium or granulations.

If the fistula tract communicates with the external environment, the fistula is called external; if it connects internal organs or cavities - internal. Fistulas can be congenital and acquired, can form independently, due to the course of a pathological process (fistulas with osteomyelitis, ligature fistulas, fistula between the gallbladder and stomach during a long-term inflammatory process), or can be created artificially (gastrostomy for feeding in case of a burn of the esophagus, colostomy for intestinal obstruction).

General principles of treatment

For necrosis, local and general treatment is carried out. At the same time, there are fundamental differences in the tactics and methods of treating dry and wet necrosis.

Treatment of dry necrosis

Treatment of dry necrosis is aimed at reducing the area of dead tissue and maximizing the preservation of the organ (limb).

Local treatment

After the formation of a clear demarcation line (usually after 2-3 weeks), necrectomy is performed (resection of the phalanx, amputation of a finger,

foot), and the incision line should pass in the zone of unchanged tissues, but as close as possible to the demarcation line.

General treatment

Colliquation N. develops in tissues rich in fluid, for example in the brain. The melting of dead masses in the focus of dry N. is called secondary colliquation.

Gangrene is necrosis of tissues that come into contact with the external environment and thereby acquire a gray-brown or black color.

Sequestrum is an area of necrotic, usually bone, tissue that has not undergone autolysis. Purulent fluid develops around the sequestrum.

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

With a favorable outcome of N., necrotic masses occur, or the N. area becomes overgrown with connective tissue and becomes encapsulated. With dry N., calcium salts () may be deposited in the dead masses. Sometimes N. is formed at the site of the outbreak (). Around the foci of colliquation N. is formed, dead masses resolve and arise. Necrotic parts of organs can be rejected ().

The outcome of N. is determined functional value dying part of the organ. In some cases, tissue damage does not leave significant consequences, in others it leads to severe complications.

Bibliography: Davydovsky I.V. General human, p. 156, M., 1969; General human pathology, ed. A.I. Strukova et al., p. 116, M., 1982.

Hematoxylin and eosin staining; ×250">

Rice. 1. Microscopic specimen of a tuberculous granuloma with caseous necrosis in the center. Hematoxylin and eosin staining; ×250.

Necrosis is the irreversible cessation of the vital activity of cells, tissues or organs in a living organism, caused by the influence of pathogenic microbes. The cause of necrosis can be tissue destruction by a mechanical, thermal, chemical, infectious or toxic agent. This phenomenon occurs due to an allergic reaction, disruption of innervation and blood circulation. The severity of necrosis depends on the general condition of the body and unfavorable local factors.

The development of necrosis is facilitated by the presence of pathogenic microorganisms, fungi, and viruses. Also, cooling in the area where there is poor circulation has a negative effect; under such conditions, vascular spasm intensifies and blood circulation is further disrupted. Excessive overheating affects the increase in metabolism and with a lack of blood circulation, necrotic processes appear.

Symptoms of necrosis

Numbness and lack of sensitivity are the very first symptoms that should be a reason to visit a doctor. Pallor of the skin is observed as a result of improper blood circulation, gradually the skin color becomes bluish, then black or dark green. If necrosis occurs in the lower extremities, then initially it manifests itself as rapid fatigue when walking, a feeling of cold, the appearance of lameness, after which non-healing trophic ulcers form, necrotizing over time.

Deterioration general condition the body comes from dysfunctions of the central nervous system, blood circulation, respiratory system, kidneys, liver. In this case, there is a decrease in immunity due to the appearance of concomitant blood diseases and. Metabolic disorder, exhaustion, hypovitaminosis and overwork occur.

Types of necrosis

Depending on what changes occur in the tissues, two forms of necrosis are distinguished:

· Coagulative (dry) necrosis - occurs when tissue protein coagulates, thickens, dries out and turns into a curdled mass. This is the result of stopping blood flow and evaporation of moisture. The tissue areas are dry, brittle, dark brown or gray-yellow in color with a clear demarcation line. At the site of rejection of dead tissue, an ulcer appears, a purulent process develops, and upon opening, a fistula is formed. Dry necrosis forms in the spleen, kidneys, and umbilical cord stump in newborns.

· Liquation (wet) necrosis - manifested by swelling, softening and liquefaction of dead tissue, the formation of a gray mass, and the appearance of a putrid odor.

There are several types of necrosis:

· Heart attack - occurs as a result of a sudden cessation of blood supply to a tissue or organ. The term ischemic necrosis means necrosis of a part of an internal organ - infarction of the brain, heart, intestines, lung, kidney, spleen. With a small infarction, autolytic melting or resorption occurs and complete tissue restoration occurs. An unfavorable outcome of a heart attack is tissue disruption, complications or death.

· Sequestrum – a dead area of bone tissue located in the sequestral cavity, separated from healthy tissue due to a purulent process (osteomyelitis).

· Gangrene – death of the skin, mucous surfaces, and muscles. Its development is preceded by tissue necrosis.

· Bedsores – occur in immobilized people due to prolonged compression of tissues or damage to the skin. All this leads to the formation of deep, purulent ulcers.

Diagnosis of necrosis

Unfortunately, patients are often sent for examination using X-rays, but this method does not allow identifying pathology at the very beginning of its development. Necrosis is noticeable on x-rays only in the second and third stages of the disease. Blood tests also do not provide effective results in investigating this problem. Modern magnetic resonance imaging or computed tomography devices today allow timely and accurate determination of changes in tissue structure.

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Outcome of necrosis

The outcome of necrosis is favorable if there is enzymatic melting of the tissue, growth of connective tissue into the remaining dead tissue, and a scar is formed. The necrosis zone may become overgrown connective tissue– a capsule is formed (encapsulation). Bone may also form in the area of dead tissue (ossification).

If the outcome is unfavorable, purulent melting occurs, complicated by the spread of the lesion - sepsis develops. Death is typical for ischemic and myocardial infarction. Necrosis of the renal cortex, necrosis of the pancreas (pancreatic necrosis), etc. etc. – damage to vital organs leads to death.

Treatment of necrosis

Treatment of any type of necrosis will be successful if the disease is detected at an early stage. There are many methods of conservative, gentle and functional treatment; only a highly qualified specialist can determine which one is best suited for the most effective result.

Skin necrosis is a pathological process that involves the death of a part of the tissue. It begins with swelling, after which denaturation and coagulation occurs, which leads to the last stage - cell destruction.

What causes skin necrosis?

There may be a couple of possible circumstances for the development of skin necrosis:

circulatory disorders;
exposure to pathogenic bacteria and viruses;
traumatic necrosis;
toxigenic necrosis;
trophoneurotic necrosis;
ischemic necrosis;
physical trauma;
chemical injury.

But skin necrosis may not be brought to the last stage of tissue death if manifestations of the disease are noticed in a timely manner.

Symptoms of skin necrosis

Among the first signs of skin necrosis are numbness of the anatomical area and lack of sensitivity. At the end of which, the affected area of the skin appears pale, which is replaced by a blue color and, ultimately, blackening with a green tint. In addition, there is a general deterioration in the patient’s condition, which manifests itself:

high temperature;
increased heart rate;
swelling;
hyperemia.

An indicator that makes past symptoms more convincing is pain under the affected area of the skin.

Skin necrosis after surgery

Skin necrosis is one of the negative consequences of poor preparation for surgery. The detrimental outcome of surgical intervention in most cases appears two to three days after the end of the operation. Superficial skin necrosis is located along the suture. The deepest necrosis of the suture contributes to its divergence, which significantly worsens the patient’s condition and complicates the course of the disease itself.

Among the circumstances of the formation of skin necrosis at the end of operations are the following:

insufficient blood supply;
large tissue detachment;
excessive seam tension;
infection of damaged skin areas.

Treatment of skin necrosis with folk remedies

To cure the disease at home, you need to prepare ointments. Among the many existing recipes, we noted two.

To make the first product you need:

Take 50 grams of wax, honey, rosin, lard, laundry soap and sunflower oil.
Place all ingredients in a saucepan, mix thoroughly and boil.
Then, allow the mass to cool and add 50 grams of finely chopped onion, garlic and aloe in that direction.
Mix everything carefully.

Before applying the ointment to the affected area, you need to warm it up.

The second recipe for a folk remedy for the treatment of skin necrosis is easier to apply:

Take one tablespoon of lard, one teaspoon of slaked lime and oak bark ash.
Mix all ingredients thoroughly.

The ointment is applied with a bandage at night and removed in the morning. The course lasts three days.

Treatment of skin necrosis depends on the form of the disease and the stage of its development. Local treatment includes two stages:

preventing the development of infection;
excision of dead tissue.

The second stage occurs only after two to three weeks of effective treatment. For non-specialized treatment, the following therapies are prescribed:

bactericidal;
detoxification;
vascular.

In addition, surgical intervention is possible, but it is used very rarely.

Doctors often have to deal with a problem such as necrosis. Types, causes and treatment of this disease can be safely classified as information relevant to modern society. After all, quite a lot of ordinary people encounter symptoms of tissue and cell necrosis. And sometimes the result of such a process can be Therefore, it makes sense to study this issue.

What is necrosis

This term implies the death of cells in the human body with the final stop of their functions. That is, life activity in a certain area of the body after the completion of necrotic processes is no longer possible.

Virtually all types of necrosis appear due to the influence of an extremely strong irritant. Sometimes a weak stimulus leads to a similar state. In this case, exposure must be prolonged to cause serious damage. As an example of slow development, it is worth citing the transformation of reversible dystrophy into irreversible. This process is divided into several key stages. We are talking about paranecrosis, when the changes are still reversible, necrobiosis (the changes are irreversible, but the cells are still alive) and necrosis, in which autolysis occurs.

Autolysis is understood as the fact of self-digestion of tissues and cells that have died due to the influence of certain enzymes. In fact, this process is very necessary for the body, since it makes possible complete healing after necrosis.

Impact of various factors

When studying this topic, it would be logical to pay attention to the factors that may cause different kinds necrosis. Their list is as follows:

Thermal. Exposure to temperatures falling below -10°C or above +60°C.

Mechanical. These are ruptures, compression, crushing.

Circulatory. We are talking about the cessation of blood supply to a certain area of the body due to obliteration of a vessel or prolonged spasm. The vessel may also be compressed too much by the tourniquet or blocked by a blood clot. The influence of the tumor cannot be ruled out.

Electrical. When in contact with current, the body can be exposed to a critical temperature, causing cell death.

Toxic. Certain types of necrosis can result from the breakdown of microorganisms or exposure to their waste products.

Neurogenic. Due to damage to the nerve trunks of the spinal cord, trophic ulcers are formed.

Chemical. This group of factors includes exposure to alkalis and acids. The former dissolve proteins and thereby cause wet colliquation necrosis. The latter cause protein coagulation and lead to the development of dry coagulation necrosis.

As you can see, a variety of factors can affect the condition of cells.

Types of necrosis

The death of tissues and cells can manifest itself in different ways. Moreover, the differences are sometimes significant. Here are the most common types of necrosis:

Gangrene. This is necrosis of tissues that come into contact with the external environment. It can be dry (coagulative necrosis) or wet (colliquative tissue destruction). There is also a gas form caused by the action of spore-forming microorganisms.

But depending on the form of the disease, treatment may differ significantly. In particular, the most common species necrosis - vascular, it requires a special approach, since we are actually talking about a heart attack.

Surgical intervention

In case of diagnosing extensive necrosis chest and limbs that significantly disrupt lymph and blood circulation, as well as innervation, necrotomy is performed. This is a dissection of tissue that has died due to frostbite, burns and other reasons. With its help you can quickly transform wet gangrene into dry.

Such excision and removal of dead tissue is carried out only after determining the boundaries of necrosis using a mechanical stimulus. This could be a touch with a metal ball, a surgical instrument, or a prick with a syringe needle.

Surgery is sometimes postponed until the necrotic tissue is completely demarcated. In parallel with this, it is necessary to carry out competent prevention of the development of wet gangrene.

In order not to encounter such a dangerous diagnosis as necrosis, you should initially take care of preventing exposure to those factors that can damage tissues and cells, thereby starting the process of their necrosis.

Results

Having examined the types of necrosis depending on the causes and other factors, we can conclude that this disease is extremely dangerous and requires high-quality quick diagnostics. Without professional treatment, the situation will be difficult to change. Therefore, the best thing to do at the first symptoms indicating necrosis is to immediately visit a doctor.

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 the life expectancy of different cells is 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 detachment of phosphate groups from nucleotides and the release of 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). With focal necrosis, complete restoration of the outer cell membrane can occur. Changes in the cytoplasm (coagulation, plasmorrhexis, plasmolysis), as well as changes in the cell nucleus, are a morphological expression of the enzymatic process, which is based on the activation of hydrolytic enzymes of lysosomes.
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 are often preserved in areas of necrosis long time, but then undergo fragmentation and clumpy 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 structural features 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 blood pigments that permeate them undergo a number of changes. In some cases, foci of necrosis are stained with bile. When putrefactively melts, dead tissue emits a characteristic foul odor.

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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

Distinguish the following types necrosis: 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, separation) - 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 (mostly dark in 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, putrefactive 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. There are 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 internal organs(stomach, intestines, liver, gallbladder, pancreas, kidney, bladder, lung, etc.) are always moist. 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:

injury, 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:

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

Classification according to clinical manifestations:

Liquation necrosis (necrotic tissue changes accompanied by edema).
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.
Gangrene.
Sequestration.
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 stroke brain. 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.
With fat necrosis, irreversible changes in adipose 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 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 circulatory problems 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 an accurate diagnosis, form and stage 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, you can use the products quite successfully traditional medicine. 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 can undergo degenerative changes - hyalinosis And petrification(see below). Sometimes it forms in the scar bone (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 condition, there is a complete or partial metabolic disorder, which sooner or later becomes the cause of their complete incapacity. The 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, the face is irreversible dystrophic changes 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– another fairly common reason that contributes to the occurrence of this condition. Quite often, this type of damage occurs as a result of exposure to chemical factors such as acid and alkali. Such infectious and non-communicable diseases how diabetes 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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