By its nature, the disease under consideration has rather serious consequences, since the result of necrosis is the death of individual (sometimes very extensive) tissue sections. As a result, the organs and systems of the patient will not be able to function fully in the future. Often, necrosis is the cause of death: pathological cells grow very quickly, so you should immediately respond to the first symptoms of the disease.

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

In its development, this ailment goes through 3 stages:

• Prenecrosis.

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

• Death of tissues.

Necrosis of the affected cells occurs.

• Destructive changes.

Pathological tissues disintegrate.

To identify necrosis, which are of a superficial nature, there are no special problems: the doctor gets acquainted with the patient's complaints, conducts blood tests, and takes a sample of fluid from the wound surface. In some cases, if gas gangrene is suspected, an x-ray of the affected area may be done (to confirm the presence of gas).

With necrosis of internal organs, the diagnostic procedure is more extensive, and may include:

• Ryen genography.

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

• Radioisotope scanning.

It is prescribed in cases where the previous diagnostic method was infertile. To carry out this procedure, the patient is injected with a medical preparation, which includes a radioactive substance. A few hours later, the zones of radioactivity are recorded in the patient's body. The area affected by necrosis, due to the lack of blood circulation in it, will be represented in the image as a "cold" spot.

• Computed tomography.

It is used at all stages if bone necrosis is suspected. At an early stage of the development of this pathology, the diagnostician during CT should pay attention to the presence of cystic cavities filled with fluid. The presence of such formations, with the infertility of previous research methods; patient complaints will help determine the diagnosis.

• Magnetic resonance imaging.

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

Necrosis treatment methods

How is the operation for necrosis?

Surgical treatment for necrosis is not shown in all cases: here everything will depend on the form of necrosis, its stage:

• Necrotomy.

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

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

Dermatoplasty should be performed after necreatomy, or (if the defective tissue is not too large in volume), sutures should be applied.

• Limb amputation / resection of the affected organ. Required under the following circumstances:

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

When a limb is amputated, resection is carried out significantly above the visible level of the lesion. The length of hospital stay following the completion of the amputation can range from 6 to 14 days. In the postoperative period, the patient must take a course of antibiotics and pain relievers. If there are no complications after the performed manipulation, after 2 weeks it is permissible to carry out prosthetics.

Amputation with necrosis is fraught with the following complications:

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

With necrosis that affect bone tissue, several types of surgical procedures can be used:

Endoprosthetics

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

Arthrodesis

This manipulation consists in resecting the bones that articulate with each other. After that, these bones are connected, thereby ensuring their fusion in the future. This procedure is fraught with negative consequences in terms of the working capacity of the operated person: it is problematic to climb / descend the stairs, sit.

4 assessments, average: 2,25 out of 5)

CHAPTER 13 NECROSIS (DEATH)

CHAPTER 13 NECROSIS (DEATH)

In a healthy human body, cell death and regeneration constantly occur: cells of the epidermis, epithelium of the upper respiratory tract slough off, blood cells are destroyed, and newly formed cells take their place, while the functions of organs do not suffer.

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

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

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

Direct necrosisarise directly in the area of ​​influence of any external factor. The death of cells can be due to the effect of mechanical force and to one degree or another is expressed both with closed (fractures, dislocations, ruptures, etc.) and with open (wounds) injuries.

Necrosis can occur with 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 vital activity of pathogenic microorganisms is one of the components of purulent diseases and complications.

Direct necrosis developing under the influence of these factors is very peculiar and is discussed in detail in the corresponding chapters of the textbook.

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

Etiology and pathogenesis of circulatory necrosis

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

tiya does not require a direct impact from the outside on a certain area of ​​the body, necrosis appears as if by themselves, due to internal causes.

Classification

The main reasons for the development of circulatory necrosis:

Violation of arterial patency;

Violation of venous outflow;

Microcirculation disorder;

Lymph circulation disorder;

Violation of innervation.

These reasons can arise acutely or gradually due to the progression of chronic diseases.

In some cases, necrosis also develops as a result of violations of systemic hemodynamics. The development of trophic ulcers (one of the types of necrosis) on the legs with arterial hypertension is described.

Acute and chronic disorders of arterial patency

Impaired arterial blood flow is the most common cause of circulatory necrosis, since a lack of oxygen and nutrients to the tissues quickly causes cell death. Violation of arterial patency can occur acutely and develop gradually.

Acute violation of arterial patency

Acute violation of arterial blood supply is most dangerous due to the development of massive tissue necrosis. In this case, there are strongest, difficult to stop pain in the limb; the skin becomes marbled (pale with bluish spots), becomes cold; often there is ischemic muscle contracture, impaired sensitivity, paresthesia. Patients are forced to lower the limb down, which, due to a slight increase in blood flow, helps to reduce pain.

The most famous classification of stages of acute ischemia, proposed by V.S. Saveliev.

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

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

The stage of organic changes. The duration of ischemia is up to 12-24 hours. Violations of tactile and pain sensitivity and limitation of movements due to muscle contracture are added to the described picture. Restoration of blood flow allows you to preserve the limb, but there is a limitation of function.

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

At 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, a threat to the patient's life is created, therefore, the main methods of treatment are necrectomy and amputation.

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

In terms of diagnostics, it is extremely important to determine the pulsation of the peripheral arteries. Its absence at a certain level makes it possible to establish a topical diagnosis of a vascular lesion.

To confirm the diagnosis and clarify the nature, localization and length of the vascular lesion, special research methods are used: rheovasography, Doppler sonography and angiography.

The main causes of acute disorders of arterial circulation:

Damage to the main vessel;

Thrombosis;

Embolism.

Damage to the main vessel

In case of trauma, the artery can be crossed, compressed by bone fragments, the formation of a pulsating hematoma, squeezing the great vessel. At the same time, the pulsation of the artery from the distal zone of injury ceases to be determined and a characteristic clinical picture of acute ischemia develops. It should be noted that with any injury there is a pronounced pain syndrome and a change in skin color in the damaged area, which can complicate the diagnosis of circulatory disorders. In this regard, it is imperative to determine the ripple of the periphery.

arteries during examination of a victim with trauma, and, if necessary, the use of special diagnostic methods.

Traumatic injuries of the arteries conditionally include the imposition of a tourniquet on the limb for a long time, as well as accidental intraoperative ligation of the artery. So, 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 the damaged main artery are the imposition of a vascular suture, prosthetics or bypass grafting of the damaged vessel.

Thrombosis

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

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

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

Embolism

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

Depending on the localization of the embolus, pulmonary embolism and embolism of the arteries of the systemic circulation (carotid, femoral, mesenteric, etc.) are isolated.

The causes of pulmonary embolism are thrombophlebitis of the veins of the systemic circulation, most often - the veins of the lower extremities 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.

Air embolism is a consequence of violation of the rules of infusion therapy, when air enters the patient's vessels. Its occurrence is also possible if the veins of the neck are damaged (they collapse poorly, and air can enter them during inhalation with negative pressure).

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

The clinical picture of thromboembolism is the sudden onset of symptoms of acute ischemia. The severity of symptoms, as well as the incidence of extensive necrosis, is greater than with thrombosis. This is due to the fact that, in most cases, emboli block the unaltered main arteries, leading to a one-stage cessation of powerful normal blood flow, and collaterals are usually not yet developed.

The method of treatment is embolectomy (except for extreme ischemia), and with a previous vascular lesion - reconstructive surgery.

Distinguish between direct and indirect embolectomy.

At straight embolectomy make an incision in the area of ​​localization of the embolus, open the artery, mechanically remove the embolus and apply a vascular suture. Currently, direct embolectomy has given way to indirect (Fogerty operation).

Advantages indirect embolectomy:

You do not need to know the exact location of the embolus;

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

The dissection of the artery is performed in the intact area, which reduces the risk of thrombosis.

To perform an indirect embolectomy, a Fogerty 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 Fogerty catheter is inserted into its lumen (Fig. 13-1).

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

The catheter is deliberately advanced beyond the zone of localization of the thrombus, with the help of a syringe with an inert solution, the balloon is inflated and the catheter is pulled out, while removing the embolus in the artery and restoring blood flow.

Chronic impairment of arterial patency

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

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

Clinical picture

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

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

I degree - the onset of pain after 500 m 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.

Complaints of patients about cold feet and lower legs, paresthesia are characteristic.

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

Objective examination reveals limb hypotrophy; reduction of hairline; limb pale, 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 region is characteristic. This is due to the greatest distance of the indicated 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, dopplerography and angiography.

Clinical differences between atherosclerosis obliterans 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 disease are presented in table. 13-1.

Table 13.1.Clinical differences between atherosclerosis obliterans and endarteritis obliterans

Treatment methods for chronic violations of arterial patency are divided into conservative and surgical.

Conservative treatment

Complex treatment is carried out. 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;

Physiotherapy effect on the lumbar sympathetic ganglia.

Surgery

Lumbar sympathectomy interrupts sympathetic innervation, reduces spastic contraction of the vessels of the lower extremities, and promotes collateral opening. Improving blood flow

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

Intimothrombectomy (endarterectomy) - removal of atherosclerotic plaque with thrombotic masses together with the intima of the vessel. It is used for local vasoconstriction due to a pathological process. Distinguish between open and semi-closed intimothrombectomy (Fig. 13-2).

Rice. 13-2.Intimotrobectomy according to Dos Santos: a - open; b - half-closed (using a loop and a deobliterotome)

Prosthetics and bypass surgery. The affected area of ​​the vessel is replaced with a prosthesis (prosthetics) or above and below the site of stenosis into the vessel

Rice. 13-3.Femoropopliteal bypass grafting with autovein

Rice. 13-4.Aorto-femoral bifurcation bypass grafting with a synthetic prosthesis

a shunt is sewn in, creating conditions for a roundabout blood flow (shunting). An autovein (large saphenous vein of the patient's thigh) or synthetic prostheses made of lavsan, velor, etc. (Fig. 13-3 and 13-4) are often used as prostheses. In some cases, an allograft from the umbilical cord vessels is used. To bypass vessels of medium and small caliber, the bypass in situ technique is used (instead of the affected artery, the blood flow is “let in” 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).

The methods of endovascular surgery are based on the introduction of special catheters and instruments into the lumen of the artery, allowing, under X-ray control, to dilate the stenotic portion of the artery (using a special catheter with a balloon at the end), laser recanalization (an atherosclerotic plaque is "burned" by a laser beam), vessel frame (stent).

Violation of venous outflow

Violation of the venous outflow, as well as the inflow of arterial blood, worsens the conditions for the vital activity of cells and tissues, but the consequences of these disorders are distinguished by a certain originality.

Differences in necrosis in violation

venous outflow and arterial blood supply

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

development of small superficial necrosis (trophic ulcers) is more characteristic, while when arterial blood supply is disturbed, extensive necrosis and gangrene of the extremities occur more often (trophic ulcers may also appear). With venous pathology, the development of gangrene does not occur without the addition of infection.

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

Localization of necrosis is characteristic. With arterial insufficiency, tissue necrosis usually begins at the tips of the fingers and the heel region, that is, in the places farthest from the heart. In case of venous insufficiency, due to the structural features of the venous bed of the lower extremities, the worst conditions for tissues are created in the region of the medial ankle and in the lower third of the lower leg, where trophic ulcers usually form.

Disorders of venous outflow can be acute or chronic.

Acute violation of venous outflow

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

For the development of necrosis, damage to the deep veins of the lower extremities is important. The defeat of 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 edema and cyanosis of the skin. The superficial veins are clearly contoured and bulge. On palpation, there is a sharp pain along the neurovascular bundle.

Similar symptoms, with the exception of pain and soreness, occur when deep veins are damaged (compressed). A clear 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 the acute period is rare.

Treatment

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

Disaggregants (acetylsalicylic acid, dipyridamole, pentoxifylline);

Anticoagulants (sodium heparin, sodium enoxaparin, phenindione);

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

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

Indications for surgery arise with thrombophlebitis of superficial veins in the following cases:

Ascending thrombophlebitis with the risk of transition of the process to deep veins and the development of thromboembolism - ligation and vein transection are performed proximally;

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

Chronic venous outflow disorder

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

Varicose veins

The clinical picture. The most typical manifestation is varicose veins: the saphenous veins in the patient's upright position bulge, tense, have a tortuous character. Patients complain of a cosmetic defect, as well as a feeling of heaviness in the limb by the end of the day, cramps at night. The disease usually progresses slowly. The slowing down of blood flow in the 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 lower leg, in the region of the medial ankle, where subsequently a focus of necrosis appears - a trophic ulcer.

To determine the tactics of treatment, special tests are used (marching, two-band tests, etc.), as well as additional methods

studies (rheovasography, Doppler sonography, X-ray contrast phlebography).

Surgery. Phlebectomy is performed - removal of varicose veins, while usually removing the main trunk of the great saphenous vein, ligating incompetent communicating veins. In case of deep vein valves failure, extravasal correction is performed using special spirals.

Sclerotherapy. 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. The main methods: wearing elastic bandages, the use of angioprotectors and venotonic drugs (diosmin + hesperidin, troxerutin).

Post-thrombotic disease

The clinical picture. Postthrombotic disease usually begins with acute deep vein thrombosis. As a result of the transferred process, the outflow through the deep veins is disturbed, which is accompanied by the appearance of edema of the limb, a feeling of heaviness in it, cyanosis. Gradually, trophic disorders 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 to ensure the outflow of blood. Subsequently, the patency of deep veins can be restored (recanalization stage).

Violation of the patency of deep veins is detected clinically, as well as using Doppler ultrasound and X-ray contrast phlebography.

Conservative treatment - the 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 (ultraviolet irradiation and laser irradiation of autologous blood, dextran [molecular weight 30 000-40 000]);

Angioprotectors and venotonic agents (diosmin + hesperidin, troxerutin).

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

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

Restoration of the patency of veins by their surgical recanalization (like 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 disorder

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

Diabetic foot

With diabetes mellitus, angiopathy gradually develops, which is 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. At the same time, 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 a special name "diabetic foot". A feature of the diabetic foot is the combination of an infectious origin and inflammation with microcirculatory necrosis, a decrease in immune and reparative processes.

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

Systemic vasculitis

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

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

Vasculitis includes periarteritis nodosa, Schönlein-Henoch disease. The treatment of these diseases is individual, using complex schemes with the use of hormonal drugs, cytostatics, immunomodulators and other drugs.

Bedsores

In decubitus ulcers, the development of necrosis due to impaired microcirculation occurs due to prolonged compression of the tissues. The diagnosis, prevention and treatment of pressure ulcers are discussed in Chapter 9. In addition, it should be noted that pressure ulcers develop not only when the patient is 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 drainage in the abdominal cavity are also commonly called bedsores, given the mechanism of their development. Prevention of bedsores of this kind - early removal of drains, the use of tubes made of inert soft materials.

Lymph circulation disorder

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

The final stage of lymphedema is fibredema (elephantiasis) of the extremities. At the same time, 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, the skin areas hang in the form of a kind of aprons. Against this background, the formation of superficial necrosis (trophic ulcers) with profuse lymphorrhea is possible. In the early stages of lymphedema, necrosis is not formed.

Innervation disorder

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

A feature of neurotrophic ulcers is a sharp suppression 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 (disturbed innervation).

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

The 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 the tactics of treatment.

Dry and wet necrosis

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

Dry (coagulation) necrosis characterized by 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 join, 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 volume of the organ, while around the foci of necrotic tissues hyperemia is expressed, there are bubbles with a transparent or hemorrhagic fluid, the outflow of turbid exudate from skin defects. There is no clear boundary between the affected and intact tissues: inflammation and edema spread beyond the necrotic tissues over a considerable distance. Attachment of a purulent infection is characteristic. With wet necrosis, severe intoxication develops (high fever, chills, tachycardia, shortness of breath, headaches, weakness, profuse sweat, changes in blood tests of an inflammatory and toxic nature), which, as the process progresses, can lead to organ dysfunction 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 by a smaller volume of dead tissues and carries a much lower threat to the patient's life. In what cases does dry necrosis develop, and in what cases does moist necrosis?

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 disturbed, which does not occur immediately, but gradually. Most often, dry necrosis develops in patients with reduced nutrition, when there is practically no fatty tissue rich in water. For the occurrence of dry necrosis, it is necessary that there are no pathogenic microorganisms in this zone, 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);

Large volume ischemia (eg, thrombosis of the femoral artery);

Severity in the affected area of ​​tissues rich in fluid (adipose tissue, muscles);

Accession of infection;

Concomitant diseases (immunodeficiency states, 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 extensiveness of the lesion, in the pathogenesis of which the vascular factor is of significant importance.

The characteristic appearance of fabrics is their black or gray-green color. This color change is associated with the decomposition of hemoglobin on 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, pancreas. Foci of necrosis in these organs outwardly look completely different.

Table 13-3.Differences between trophic ulcers and wounds

The defeat of the whole organ or most of it. The development of gangrene of the finger, foot, limb, gallbladder, lung, etc. is possible. At the same time, gangrene of a limited part of the body, the dorsum of the finger, etc. cannot be developed.

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

Trophic ulcer

Trophic ulcer is a superficial defect of integumentary tissues with possible damage to deeper tissues, which does not tend to heal.

Trophic ulcers are usually formed with chronic circulatory and innervation disorders. By etiology, atherosclerotic, venous and neurotrophic ulcers are distinguished.

Considering that with a trophic ulcer, as well 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. The healing process is usually 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 tissues is usually called a trophic ulcer.

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

Fistulas

Fistula is a pathological course in tissues connecting an organ, a natural or pathological cavity with the external environment, or organs (cavities) with each other.

The fistulous passage is usually lined with epithelium or granulations.

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

These examples show how varied fistulas can be. Their features, methods of diagnosis and treatment are associated with the study of diseases of the corresponding organs and are the subject of private surgery.

General principles of treatment

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

Dry necrosis treatment

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

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

feet), while the cut line should pass in the area of ​​unaltered tissues, but as close as possible to the demarcation line.

General treatment

With dry necrosis, general treatment is primarily etiotropic, it is aimed at the underlying disease that caused the development of necrosis. This treatment allows you to limit the area of ​​necrosis to a minimum amount of tissue. The most effective measures should be taken. If it is possible to restore blood supply by intimothrombectomy, 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).

Antibiotic therapy is of great importance for the prevention of infectious complications.

Treatment of wet necrosis

Wet necrosis, accompanied by the development of infection and severe intoxication, pose an immediate threat to the patient's life. Therefore, with their development, a more radical and vigorous treatment is necessary.

At an early stage, the goal of treatment is to try to convert wet necrosis to dry necrosis. If the desired result cannot be achieved or the process has gone too far, the main task is to radically remove the necrotic part of the organ (limb) within the bounds of known healthy tissues (high amputation).

Early treatment Local treatment

To convert wet necrosis to dry necrosis, topically use the washing of the wound with antiseptics (3% hydrogen peroxide solution), opening the streaks and pockets, draining them, dressings with antiseptic solutions (boric acid, chlorhexidine, nitrofural). 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 conduct powerful antibiotic therapy, including intra-arterial antibiotics. Given 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, 1-2 days are taken to try to convert wet necrosis to dry, although in each case the issue is decided individually. If, during treatment, edema decreases, inflammation subsides, intoxication decreases, the number of necrotic tissues does not increase, conservative treatment can be continued. If after a few hours (or in a day) it is clear that there is no effect of treatment, inflammatory changes progress, necrosis spreads, intoxication grows, then the patient should be operated on, since this is the only way to save his life.

In cases where the patient is admitted to the hospital with wet gangrene of the limb, severe inflammation and severe intoxication, it is not necessary to try to convert wet necrosis to dry, short-term preoperative preparation (infusion therapy for 2 hours) should be carried out and the patient should be operated on for emergency indications.

In case of wet necrosis, surgical treatment consists in the removal of necrotic tissues within the bounds of known healthy, unaltered tissues. In contrast to dry necrosis, given the high severity of the inflammatory process, the addition of infection, in most cases, high amputation is performed. So, with wet foot necrosis, for example, with the spread of hyperemia and edema to the upper third of the lower leg (a fairly common situation), amputation should be performed on the thigh, and preferably at the level of the middle third. Such a high level of 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) is very likely, which significantly worsen the general condition of the patient and the prognosis for his recovery. In some cases, an even higher amputation has to be repeated.

Treatment of trophic ulcers

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

For trophic ulcers, local and general treatment is used.

Local treatment

In the local treatment of trophic ulcers, the surgeon has three tasks: fighting the infection, cleansing the ulcer from 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 alcoholic tincture of iodine, the ulcerative surface itself is washed with a 3% solution of hydrogen peroxide and dressings are applied with an antiseptic solution (3% boric acid solution, an aqueous solution of chlorhexidine, nitrofural).

Cleansing from necrotic tissue

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

The peculiarity of trophic ulcers is that at no stage of treatment should ointment dressings be used!

Defect closure

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

solution of brilliant green or 5% solution of potassium permanganate, causing the formation of a scab, under which epithelization will subsequently occur. The use of gel (iruksol) also contributes to epithelization.

To close the ulcer defect after it has been cleared, in some cases, free skin grafting or excision of the ulcer with plasty with local tissues can be used. However, these measures should be carried out after targeted exposure to the cause of the ulcer.

For the healing of venous (but not atherosclerotic!) Trophic ulcers is effective compression therapy. Compression therapy of trophic ulcers is understood as the imposition of a zinc-gelatin bandage on the limb, for which various modifications of the Unna paste are used. Rp .: Zinci oxydati

Gelatinae ana 100.0

Glycerini 600.0

Aqua destil. 200.0

M. f. pasta.

Dressing technique. The patient is placed on the table, the lower limb is raised, after which the paste is applied with a brush in a heated form from the base of the fingers to the upper third of the leg (including the trophic ulcer zone). This is followed by a layer of gauze bandage. Then again apply a layer of paste with a brush, soaking the bandage with it. In total, 3-4 layers of bandage 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 ulcer surface are epithelized.

Compression therapy significantly increases the ability to close 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 in various ways to improve blood circulation. In this case, both conservative and surgical methods are used. So, 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 the

Details

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

The necrotic process goes through a series stages :

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

Microscopic signs of necrosis:

1) Kernel changes

1. Karyopyknosis- shrinking of the kernel. At this stage, it becomes intensely basophilic - hematoxylin turns dark blue.
2. Karyorexis- disintegration of the nucleus into basophilic fragments.
3. Karyolysis- core dissolution

Pycnosis, rexis and lysis of the nucleus follow 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 karyopycnosis.

2) Changes in the cytoplasm

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

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

3) Changes in the intercellular substance

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

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

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

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

With tissue necrosis, their texture, color and odor change. The tissue can become dense and dry (mummification), it can 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, skin often becomes gray-green, 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 action on the tissue of physicochemical factors (radiation, temperature, electricity, etc.)

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

2) toxic necrosis

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

Example: necrosis of cardiomyocytes when exposed to diphtheria exotoxin.

3) trophoneurotic necrosis

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

Example: bedsores.

4) allergic necrosis

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

Example: the Arthus phenomenon.

5) vascular necrosis- heart attack

It occurs when the blood flow in the arteries is disturbed or stopped due to thromboembolism, 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 due to the direct effect of a pathogenic factor.

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

Clinical and morphological forms of necrosis.

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

1) coagulation (dry) necrosis

Dry necrosis is based on the processes of protein denaturation with the formation of poorly soluble compounds that may not undergo hydrolytic cleavage for a long time.

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

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

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

Examples:

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

Heart attack

Caseous (cheesy necrosis) with syphilis, tuberculosis

Dry gangrene

Fibrinoid - connective tissue necrosis, 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 a homogeneous necrotic material of bright pink color, which is similar (!) To fibrin.

2) colliquation (wet) necrosis

It is characterized by the melting of dead tissue, the formation of cysts. It develops in tissues that are relatively poor in protein 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 of:

Ischemic cerebral infarction

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

3) gangrene

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

a) dry gangrene

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

Necrotic tissue dries up, shrinks and hardens under the influence of air, they are clearly demarcated from viable tissue. On the border with healthy tissues, demarcation inflammation occurs.

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

Example: - gangrene of the limb with atherosclerosis and thrombosis

In case of frostbite or burns

b) wet gangrene

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

The tissue swells, becomes edematous, fetid.

Disorders of blood circulation, lymph circulation contribute to the occurrence of wet gangrene.

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

Examples of:

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

Pressure ulcers. A bedsore is the death of superficial areas of the body that are exposed to pressure.

Noma is a watery cancer.

c) gas gangrene

It occurs when a wound is 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 frequent clinical symptom is crepitus.

4) sequester

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

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

Soft tissue

5) heart attack

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

a) forms of heart attack

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

Less often, necrosis has an irregular shape. Such necrosis occurs in the heart, intestines, that is, in those organs where non-trunk, loose or mixed type of arterial branching prevails.

b) value

A heart attack can cover most or all of an organ (subtotal or total infarction) or is 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 corolla

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

- red (hemorrhagic)

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

Clinical manifestations of necrosis.

1) systemic manifestations: fever, neutrophilic leukocytosis. Intracellular enzymes are determined in the blood: the MB isoenzyme of cratin 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 delimits the dead tissue from the healthy one. In this zone, the blood vessels expand, plethora and edema occur, and a large number of leukocytes appear.

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 petrification. Bone formation at the site of necrosis.

6) purulent fusion

This is the purulent fusion of heart attacks in sepsis.

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 - this is the destruction of cells.

Why does skin necrosis develop?

There can be several reasons for the development of skin necrosis:

• the action of pathogenic bacteria and viruses;
• traumatic necrosis;
• toxigenic necrosis;
• trophoneurotic necrosis;
• ischemic necrosis;
• physical injury;
• chemical injury.

But skin necrosis can not be brought to the last stage of tissue death if the manifestations of the disease are noticed in time.

Skin necrosis symptoms

Among the first symptoms of skin necrosis are numbness of the anatomical area and lack of sensitivity. After that, the pallor of the affected area of ​​the skin appears, which is replaced by a blue color and, ultimately, blackening with a green tint. There is also a general deterioration in the patient's condition, which is manifested by:

• high fever;
• increased heart rate;
• swelling;
• hyperemia.

The symptom that makes the previous symptoms more persuasive 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 result of surgery usually appears two to three days after the surgery. Superficial necrosis of the skin is located along the seam. Deep suture necrosis contributes to its divergence, which significantly worsens the patient's condition and complicates the course of the disease itself.

Among the reasons for the formation of skin necrosis after operations are noted:

• insufficient amount of blood supply;
• significant tissue detachment;
• excessive tension on the seams;
• infection of damaged skin areas.

Treatment of skin necrosis with folk remedies

In order to cure the disease at home, it is necessary to prepare ointments. Among the many existing recipes, we have noted two.

To prepare the first product, you must:

1. Take 50 grams of wax, honey, rosin, lard, laundry soap and sunflower oil.
2. Put all the ingredients in a saucepan, mix thoroughly and boil.
3. After that, let the mass cool and add 50 grams of finely chopped onions, garlic, etc.
4. Mix everything thoroughly.

Before applying the ointment to the affected area, it is necessary to warm it up.

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

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

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

Drug treatment

Causes of necrosis

Necrosis is an 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 mechanical, thermal, chemical, infectious and toxic agents. This phenomenon occurs as a result of an allergic reaction, impaired 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, viruses. Also, cooling in the area where there is a violation of blood circulation has a negative effect, in such conditions vasospasm increases and blood circulation is even more disturbed. Excessive overheating affects an increase in metabolism and with a lack of blood circulation, necrotic processes appear.

Necrosis symptoms

Numbness, lack of sensitivity is the very first symptom that should be a reason for visiting a doctor. Pallor of the skin is observed as a result of improper blood circulation, gradually the skin color becomes cyanotic, then black or dark green. If necrosis occurs in the lower extremities, then at first it is manifested by rapid fatigue when walking, a feeling of coldness, the appearance of lameness, after which non-healing trophic ulcers form, which necrotize over time.

Deterioration of the general condition of the body occurs 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. There is a metabolic disorder, exhaustion, hypovitaminosis and overwork.

Types of necrosis

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

· - occurs when tissue protein curls up, thickens, dries up and turns into a curd mass. This is the result of the cessation of blood flow and evaporation of moisture. At the same time, the areas of tissue are dry, brittle, dark brown or gray-yellow in color with a clear demarcation line. At the site of the rejection of dead tissue, an ulcer occurs, a purulent process develops, is formed, and a fistula is formed upon opening. Dry necrosis is formed in the spleen, kidneys, umbilical cord stump in newborns.

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

There are several types of necrosis:

· - occurs as a result of a sudden cessation of blood supply in the focus of tissue or organ. The term ischemic necrosis means necrosis of a part of an internal organ - infarction of the brain, heart, intestines, lungs, kidneys, spleen. With a small infarction, autolytic fusion or resorption occurs and the tissue is completely restored. An unfavorable outcome of a heart attack is a violation of the vital functions of the tissue, complications or death.

· - a dead piece of bone tissue is located in the sequestral cavity, separated from healthy tissue due to a purulent process (osteomyelitis).

· - necrosis of the skin, mucous surfaces, muscles. Its development is preceded by tissue necrosis.

· - occur in immobilized people due to prolonged squeezing 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 an examination performed using an X-ray, but this method does not allow detecting pathology at the very beginning of its development. Necrosis on X-rays is noticeable, only in the second and third stages of the disease. Blood tests also do not provide effective results in investigating this problem. Modern devices for magnetic resonance imaging or computed tomography today make it possible to timely and accurately determine changes in the structure of the tissue.

Outcome of necrosis

The outcome of necrosis is favorable if there is an enzymatic melting of the tissue, the germination of connective tissue into the remaining dead tissue, and a scar is formed. The zone of necrosis can be overgrown with connective tissue - a capsule is formed (encapsulation). Bone can also form in the area of ​​dead tissue (ossification).

With an unfavorable outcome, purulent fusion occurs, complicated by the spread of the focus - sepsis develops.