Treatment of necrosis. Tissue necrosis: causes, treatment Dry skin tissue necrosis treatment

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

Causes of necrosis

Most often lead to the development of necrosis:

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

Classification

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

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

Colliquation necrosis (necrotic tissue changes are 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.
Sequester.
Heart attack.

Symptoms of the disease

The main symptom of the pathology is the lack of sensitivity in the affected area. With superficial necrosis, the color of the skin changes - at 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 complain of lameness, convulsions, and trophic ulcers. Necrotic changes in the internal organs lead to a deterioration in the general condition of the patient, the functioning of individual body systems (CNS, digestive, respiratory, etc.)

With colliquation necrosis, the process of autolysis is observed in the affected area - decomposition of tissues under the action of substances secreted by dead cells. As a result of this process, capsules or cysts filled with pus are formed. The most characteristic picture of wet necrosis for tissues rich in fluid. An example of colliquative necrosis is an ischemic stroke of the brain. Diseases accompanied by immunodeficiency (oncological diseases, diabetes mellitus) are considered predisposing factors for 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, 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 fatty tissue occur as a result of injury or exposure to enzymes of damaged glands (for example, in acute pancreatitis).

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

There are several types of gangrene:

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

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

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

Outcome of the disease

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

Diagnostics

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

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

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

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

Treatment of necrosis

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

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

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

The cause of tissue necrosis is a malnutrition of a certain tissue area due to trauma or its putrefactive inflammation, and more often the combined effect of both. This happens due to the impact on the cells of mechanical force (ruptures, compression), as well as due to developing infection and high or low temperatures.

Any tissues and organs can become necrotic. The speed and extent of the spread of necrosis is influenced by the ongoing mechanical impact, the addition of infection, as well as the features of the anatomical and physiological structure of the damaged organ.

To begin the manifestation of the development of necrosis, severe pain is characteristic, the skin becomes pale and cold and takes on a marble appearance. There is numbness and sensitivity is lost, the function is disturbed, although its manifestations are possible for some time after ascertaining necrosis. The necrosis begins from the lower sections and gradually spreads to the level of malnutrition, and then a line called "demarcation" is determined on the border of dead and living tissues. The presence of demarcation indicates the possibility of performing an operation - removing the necrotic part along this line or above it. This long-established rule of tactics among surgeons is the only correct one that meets today's ideas.

Therapeutic measures are aimed at maintaining the general condition using active infusion therapy (blood, blood substitutes, antibiotics, vitamins, etc.).

Local treatment consists in removing necrosis within healthy tissues, and the amount of surgical intervention depends on the type of gangrene, which is dry and wet. Dry proceeds favorably, and surgical intervention is indicated when a demarcation line is formed. With wet gangrene, when general manifestations are pronounced, accompanied by severe intoxication, an immediate amputation of the limb is carried out within healthy tissues, that is, above the level of the necrosis border.

It is known that more differentiated tissues are affected much earlier. Therefore, with necrosis of the muscles and skin, the tendons and bones are in a relatively unaffected state. During surgical intervention, it is necessary to take into account this phenomenon and not to remove necrotic areas to the full depth, but to excise only the affected ones (do not excise the bone tissue regardless of the state of viability) with replacement with a full-fledged skin-subcutaneous pedicled flap. Purulent complications should be eliminated by regional infusion of antibiotics.

When unaffected bones and tendons are identified, they are closed with plastic material according to one of the existing methods. In such cases, it is possible to save the segment of the limb and prevent the disability of the victim. There were 11 such patients.

All of them were operated on according to the technique adopted by us, which consisted in catheterization of the main vessel, removal of necrotic soft tissues with replacement of the soft tissue defect with a pedicle flap.

5 of them had damage to the lower leg, two to the foot, one to the forearm, and three to necrosis of the hand.

All patients had a very severe injury with damage to soft tissues and bones, in 2 patients with a closed fracture of the tibia, as a result of improper treatment (a circular plaster bandage was applied), necrosis of the tibia occurred, which required necrectomy of the segment.

One patient admitted 3 days after the injury of the forearm had signs of segment necrosis at the level of the fracture. Another patient has necrosis of the calcaneus and talus, which were removed during the treatment.

Three patients had an open fracture of the lower third of the leg bones with an acute purulent complication and necrosis of the tibia within 10-15 cm.

One patient, whose hand was under pressure, developed soft tissue necrosis of the hand and other injuries. All patients required a non-standard approach to rehabilitation treatment.

Since the degree of damage and affection of the patients under consideration is very diverse, and systematization is difficult, as an illustration, we will give several different types of lesions.

An example would be patient B., aged 26.

While working on the press, the right hand fell under it. The patient was taken to the surgical department of the regional hospital.

It was necessary to take into account the mechanism of formation of a wound around the hand, caused by compression by the press and arising along the edge of its impact. It could be assumed that the soft tissues were so affected that it was impossible to count on their recovery after exposure to a two-ton press. The resulting wound at the level of the wrist joint from the back surface and along the upper groove from the palmar side was sutured tightly, a plaster splint was applied.

Within a few days, the phenomena of necrosis of the damaged area of the hand and signs of severe intoxication were clearly indicated.

She was admitted to the regional hospital from the Central District Hospital, where the amputation of the hand and the formation of a stump were proposed, in a serious condition. The right hand on the rear from the level of the wrist joint, on the palmar surface from the upper palmar groove - necrotic. In the indicated area, the skin is black, hard in places, all types of sensitivity are absent, there is profuse purulent discharge from under the scab and from the wound. When the scab is cut, there is no bleeding, but copious fetid pus is released. The function of the brush is completely broken. Radiography - no bone changes, sowing detritus on the flora and sensitivity to antibiotics.

Diagnosis: severe injury with crushing and necrosis of part of the hand and 2nd, 3rd, 4th, 5th fingers of the right hand.

Operated. The brachial artery was catheterized through a.Collateralis ulnaris superior and infusion of penicillin 20 million units was started. in the infusate.

A day later, rather loosely, in the form of a “glove”, necrotic soft tissues of the hand and fingers were removed. Excised necrotic, already darkened ends of the distal phalanges (Fig. 1).

The tendons of the deep flexors and extensors are sutured over the butt of the treated phalanges.

After excision of necrotic tissues and dressing of the wound of the hand, a skin-subcutaneous-fascial flap was cut out in the area of the chest and abdomen according to the size of the defect of the hand and fingers, which were placed in this flap (Fig. 2).

Four weeks after the operation, the pedicle of the transplanted flap was cut off. Hand after cutting off the feeding leg. After wound healing, the patient was discharged home.

The infusion of antibiotics into the artery continued for 40 days with breaks between surgical interventions for two weeks. Two months after the healing of the wounds, the second finger was formed, and after the healing of the wounds, the patient was discharged and started to work (Fig. 4, 5).

Thus, our tactics with the use of plastic techniques under the guise of a long-term regional administration of antibiotics made it possible to preserve the function of the hand to a certain extent and, most importantly, prevent the disability of a still young woman.

In all patients, the engraftment of the flap occurred, in some with phenomena of marginal necrosis, followed by wound healing on its own, or with the addition of a split skin flap.

A complex subgroup of patients with tissue necrosis were patients with necrosis of more deeply located bone tissue.

The previous experience gained in the treatment of patients with soft tissue necrosis made it possible to reconsider the attitude towards the separation of the necrotic part of the limb, that is, not to carry out its amputation.

It is known from practical surgery and scientific research (M. V. Volkov, V. A. Bizer, 1969; S. S. Tkachenko, 1970; M. V. Volkov, 1974; T. P. Vinogradova, G. I. Lavrishcheva, 1974; I. V. Shumada et al. 1985) that transplanted preserved bone allografts, which initially perform a fixing role, then turn into normal bone, and subsequently perform a stabilizing and functional support role.

The process of restoring the bone to a normal functional state, depending on the properties of the graft, is not the same. In particular, T. P. Vinogradova, G. I. Lavrishcheva (1974) in their fundamental work clearly differentiated the activity of regeneration depending on the characteristics of the graft. The most active in regeneration and effective in the treatment of patients with bone defects is an autograft, in second place is a frozen allograft, and then lyophilized.

These ideas forced us to think about the advisability of using an autograft as a plastic material, and its source should be a non-rejected necrotic fragment in severe open fractures of the long bones of the extremities. This method was used in the treatment of 11 patients with severe limb injuries with purulent complications and necrosis of soft tissues and bones.

An application for an invention was submitted and a patent was received for “METHOD FOR THE TREATMENT OF OPEN INFECTED FRACTURES WITH NECROSIS OF SOFT TISSUES AND BONES” No. 2002455, 1995.

inventions. Upon admission, the patient is examined. Conduct clinical, laboratory, bacteriological, functional, radiological and other types of research.

The main artery is catheterized and antibiotics are administered as part of the infusate. After the elimination of inflammation, necrotic soft tissue formations are excised. They provide fixation with the help of author's fixators (extrafocal-compression-distraction or rod devices) or immobilization with a plaster cast.

Bone fragments are processed to create contact - with a transverse fracture in the end part, and with oblique fractures - according to its shape, but ensuring maximum contact of the bone fragments with fixation with the named fixators.

The existing soft tissue defect is replaced with a pedicled flap, for the lower limb, from the opposite leg, and for the upper limb, from the abdominal region.

After the engraftment of the flap, after 30 days from the moment of replacement of the defect, the feeding leg of the flap is cut off. Plaster immobilization or fixation with a compression-distraction apparatus is carried out until complete consolidation.

An illustration of the application of the method can serve as a patient K. 35 years old.

Entered three weeks after an open comminuted fracture of both bones of the right leg in the middle third, with displacement of fragments.

He was treated at the regional hospital. Osteomyelitis of the right leg developed with tissue necrosis and a defect of 6x8 cm with necrosis of the ends of tibial fragments and pin osteomyelitis of the calcaneus as a result of skeletal traction. Phenomena of the general inflammatory reaction.

X-ray showed a spiral comminuted fracture of both bones of the lower leg with displacement of fragments.

Operated. The femoral artery was catheterized through the returning iliac artery. Introduced 10 million units. penicillin. Soft tissue necrectomy. The pointed non-viable ends of the proximal and distal fragments about 1 cm were excised to create supportive congruence. There is no bleeding on the sawdust of the bone on both sides, the bone is white. Fragments taken for research. The ends of the fragments of the tibia are devoid of periosteum about 5 cm above and below, the fragments are pale grayish in color.

The bone fragments were compared end to end and fixed using the Ilizarov apparatus.

Infusion of antibiotics for a week, followed by plasty of the soft tissue defect with covering of exposed fragments of the tibia with a skin-subcutaneous-fascio-muscular flap cut from the opposite leg.

The transplanted flap took root, the pedicle was cut off after 32 days. The Ilizarov apparatus was removed after 2 months. A circular plaster bandage was applied.

X-ray four months after the start of treatment showed that the fragments had grown together. Permissible load on the leg.

Morphological examination of bone tissue taken during excision of fragments.

Morphological picture of the state of viability of bone tissue.

We studied 16 preparations taken from patients with an open complicated fracture of long bones with necrosis of soft tissues and adjacent bone.

Fragments of the proximal and distal fragments of a broken bone were taken. Fixed in 12% neutral formalin solution. After decalcification in a 5% solution of nitric acid and celloidin, sections were made, which were stained with hematoxylin and according to Van Gieson.

Bone tissue is devoid of osteocytes, homogeneous in places, gluing lines are not contoured. Tinctorial properties are sharply violated. Zones of basophilia alternate with areas of oxyphilic coloration. In some places, foci of complete necrosis of bone tissue (melting bone) are visible. The process of osteogenesis is not expressed. Between the areas of necrotic bone in some preparations, the formation of scar tissue is visible, in which lymphoid infiltrates with the presence of plasmocytes are traced.

In connection with the non-standard tactical and surgical decisions, we will dwell in more detail on the discussion of patients in this group.

Two patients were admitted with pronounced necrosis of the lower leg, and necrosis of the forearm - one. There were no doubts about the actions, the plans were to save the knee joint in case of damage to the lower leg and the elbow joint in case of damage to the forearm, which was quite successfully succeeded.

In all patients operated on by the proposed method, bone fragments were consolidated and the function of the leg or arm was restored, depending on the initial damage to the limb. Most importantly, the necrotic bone was not excised. She played the role of an autograft. Thus, the terms of treatment of patients were reduced several times in comparison with traditional methods of treatment, even with the currently recognized most progressive method of bilocal osteosynthesis, with all the possibilities of which it takes at least two years to correct the length of a limb segment with a bone defect of 10 cm.

If you wish to become more familiar with traumatological and orthopedic problems and the possibility of solving them, you can order books reflecting our experience.

Skin necrosis is an irreversible process of death of living cells. It develops after primary damage as a result of which blood circulation is disturbed. The disease is very dangerous and needs to be monitored by doctors. It is worth noting that the disease can be of different types.

Reasons for the development of necrosis

The condition can start after tissue damage in the following ways:

tissue necrosis

traumatic;
toxic;
trophoneurotic;
infectious-allergic diseases, as a result of which fibroid necrosis may occur;
vascular.

Traumatic

A typical case of traumatic necrosis due to frostbite, less often can be caused by: burns, injury, electric shock or radioactive radiation. It is expressed in a change in skin color to pale yellow, the tissues are dense to the touch, later vascular thrombosis is formed. In case of damage to large areas of the epidermis, a person may have a fever, decrease appetite, and regular vomiting will appear.

Toxic

It is formed due to the influence of toxins on the epidermis. It is more often formed with syphilis, diphtheria, leprosy. Toxic, epidermal necrolysis may appear as a result of exposure to the skin of medicines, alkalis, acids.

Trophoneurotic

It is provoked by a malfunction of the central nervous system. This type includes bedsores, which manifest themselves as a change in the color of the epidermis, numbness, redness and the appearance of a bubble with liquid, then the process fester.

Allergic

This species can threaten people with allergic reactions. Polypeptide protein injections become irritants.

Vascular

It occurs due to a violation of blood circulation in the arteries, due to blockage of blood vessels. Almost all internal organs can be exposed to this type.

Tissue death can begin after bedsores and non-healing ulcers. Violation of blood microcirculation in tissues can cause a heart attack, diabetes mellitus, injuries of the spinal cord and large vessels

Symptoms

Tissue necrosis begins to manifest itself with numbness of the affected area, its color becomes pale and shiny, which highlights the process that has begun against the background of a healthy epidermis. The process that has begun is easiest to stop and restore blood circulation, if this is not done, then the damaged areas turn blue and then turn black.

Other clinical manifestations include:

convulsions;
temperature;
loss of appetite;
general weakness;
lameness
trophic ulcers.

Before necrosis, the affected cells go through several stages:

Paranecrosis is a reversible change, a state in which the cell is in agony.
Necrobiosis is a period of cell disease that cannot be changed.
Apoptosis is the process of death.
Autolysis - decomposition.

Regardless of where the pathology is formed, the patient's internal organs are disrupted: kidneys, liver, lungs. This is due to a decrease in the immune system, metabolic disorders, which lead to hypovitaminosis and exhaustion.

Types of necrosis

Colliquation necrosis

This type is called wet, the affected tissues are flabby with the presence of pathogenic microorganisms in them. In terms of symptoms, it is similar to wet gangrene, the difference of the latter is that tissue liquefaction occurs a second time due to the addition of pyogenic bacteria. Colliquation necrosis develops very quickly, a person has collateral hyperthermia.

coagulative necrosis

This type is called dry and mainly spreads to protein-filled organs: kidneys, adrenal glands, spleen, myocardium.

The state is also divided into the following types:

View	Description
Caseous necrosis	Converts the affected cells into a curdled mass, the reasons for this are: tuberculosis, syphilis and a special type of fungus
Zenker's view	It affects the muscle mass and has a gray-yellow color with a greasy sheen. Occurs with typhus, typhoid fever, convulsions, injuries
fibrinoid	It is characterized by the fact that the affected areas are impregnated with fibrin. Often becomes a consequence of rheumatic diseases, fibroid swelling, organ dysfunction
fatty form	It is localized in the pancreas, in the retroperitoneum, in the fatty cover of the epicardium, in the layer under the paleopleura, in the subcutaneous fatty tissue, in the bone marrow

Gangrene

Photo: gangrene

The foci are black and dark green in color. Depending on the type of infection, it is dry, wet and gas. It is more often observed on the limbs, before its appearance they become inactive, the skin becomes numb and dries, hair falls out. Basically, preliminary diagnoses are atherosclerosis, endarteritis and others. Then the site begins to hurt as long as there are living cells on it, after which the sensitivity completely disappears.

Joint necrosis

In addition to the skin, pathology can affect the articular tissues, mainly the head, which occurs due to a lack of nutrients supplied to it. Causes can be physical trauma, arterial thrombosis, bad habits, and certain medications. The main symptom is the appearance of a sharp pain, the last stage leads a person to disability. A common example of joint necrosis is aseptic necrosis of the femoral head.

heart attack

Ischemic necrosis is the most common form, it becomes a consequence of ischemia. It is formed in the heart muscle, lungs, kidneys, spleen, brain, intestines, etc. Distribution options: the entire organ, part of the organ, can only be seen with a microscope (microinfarction).

Sequester

A sequester is an affected area with pus, located among healthy skin, more often a bone fragment is damaged in osteomyelitis, but may be lung tissue, muscles or tendons.

Hemorrhagic pancreatic necrosis

This is a severe pathology of the pancreas. It develops in the acute stage of pancreatitis or in chronic inflammation of the organ. It is manifested by severe pain in the region of the left rib, can be given to the lower back, chest, shoulder. There is nausea, tachycardia, temperature, red-blue spots form on the sides. With symptoms of pancreatic necrosis, the patient is brought by ambulance to a medical facility.

Diagnosis and treatment of skin necrosis

Superficial necrosis is diagnosed based on the patient's complaints, blood and fluid tests from the affected area.

To recognize the pathology of internal organs appoint:

x-ray;
radioisotope scanning;
computed and magnetic resonance imaging.

When choosing a treatment, doctors take into account the type, form of the disease, stage, as well as the presence of other diseases. Treatment of the skin is carried out under the supervision of an infectious disease specialist, resuscitator and surgeon.

Apply intravenous therapy with penicillin, clindomycin, gentamicin. Appropriate antibiotics are selected according to microbiological data. Conduct infusion therapy and stabilize hemodynamics. The affected parts of the skin are removed surgically.

Treatment of aseptic necrosis of the femoral head

With the destruction of the bone mass, medical and surgical treatment is carried out. Aseptic necrosis of the head of the hip joint requires bed rest and walking with a cane so as not to burden the affected area.

In the treatment used:

Vascular drugs (Curantil, Trental, Dipyridamole, etc.)
Calcium metabolism regulators (Ksidifon, Fosamax)
Calcium with vitamin D and mineral preparations (Vitrum, Osteogenon, Aalfacalcidol)
Chondoprotectors (Artra, Don, Elbona)
Non-steroidal anti-inflammatory drugs (Ibuprofen, Diclofenac, Naklofen)
Muscle relaxants (Mydocalm, Sidralud)
B vitamins

All medical devices are selected exclusively by a doctor, self-treatment is unacceptable. If the drugs are not effective, and aseptic necrosis of the femoral head progresses, surgery is performed.

Treatment of hemorrhagic pancreatic necrosis

Treatment takes place in the hospital, mainly in the intensive care unit.

For pain relief, they use: No-shpa, Ketons, Platifillin, Hydrotartate. The removal of pain is also facilitated by the introduction of injections of Novocain, as well as Pomedol with Atropine Sulfate and Diphenhydramine.
Antibiotics are prescribed: Cefalexin, Kanamycin.

Based on the condition of the patient, doctors decide on the operation. Without infection, the patient is given laparoscopic or percutaneous drainage of the peritoneal area. With a large amount of inflammatory fluid, you need to cleanse the blood. In the presence of an infection, part or all of the pancreas is removed.

Complications and preventive measures

The outcomes of necrosis are positive, in the case of enzymatic fusion of lesions and germination of connective tissue, scarring. Complications are purulent fusion, bleeding, sepsis.

If the treatment of necrosis of the head of the hip joint is later, the consequences threaten with disability. For the purpose of prevention, timely treatment of acute chronic diseases, reduction of trauma, strengthening of the vascular and immune systems are carried out.

Lethal outcome is typical for ischemic strokes, myocardial infarctions and other lesions of internal organs.

A normal healthy organism, faced with an attack of pathogenic microbes, launches all kinds of immune reactions designed to cope with pathological particles and protect the body from their aggressive effects. However, in certain cases, this process occurs with violations. In these cases, microbes can cause serious destructive reactions and even death of tissue cells. This process is called necrosis, it can develop as a result of the influence of external or internal factors. This condition is more than dangerous for the body and requires extremely careful treatment under the supervision of qualified professionals.

How does tissue necrosis manifest itself? Symptoms

The main symptom that should alert the patient is a feeling of numbness, as well as the absence of any sensitivity. The skin in the affected area is painted in pale tones, the appearance of deathly pallor and the appearance of waxy skin are recorded. If at this stage no measures are taken to treat pathological processes, in other words, to restore full blood circulation, then the skin will become cyanotic. It will begin to turn black or green rather quickly.

In the event that necrosis, in other words gangrene, threatens the lower extremities, patients complain of a quickly emerging feeling of fatigue while walking. At the same time, the patient's legs are constantly cold, even if the weather is hot outside. Over time, these symptoms are joined by convulsions that develop while walking. They can cause intermittent claudication - at first, a spasm affects one limb, and then it passes to the second. As pathological processes develop, trophic ulcerative lesions appear on the skin, which quickly necrotic. It is after this that gangrene develops directly.

The general deterioration of the patient's body is due to violations of the functional activity of the nervous system, as well as blood circulation. Pathological processes, regardless of the localization of necrosis, adversely affect the functioning of the respiratory system, as well as the kidneys and liver. The patient's immunity is significantly reduced, since the processes of tissue death cause concomitant blood ailments and anemia. There is a disorder of metabolic processes, which leads to exhaustion and hypovitaminosis. Against the background of all this, the patient develops constant overwork.

There are several variants of necrosis, which differ in their manifestations. We have already mentioned gangrene, which is accompanied by the death of the epidermis, as well as the mucous surfaces and muscle tissues.

A heart attack appears as a result of a sudden cessation of blood circulation in the area of \u200b\u200bthe tissue or organ. So ischemic necrosis is the death of a part of some internal organ, for example, a heart attack of the brain, heart, or intestines and other organs.

If the infarction was small, autolytic melting or tissue resorption and repair occurs. However, an unfavorable course of a heart attack is also possible, in which the vital activity of the tissue is disrupted, or complications and even death occur.

Necrosis can also take the form of sequestration, when dead parts of the bone tissue are localized inside the sequester cavity and separated from healthy tissues due to the course of a purulent process, with a disease such as osteomyelitis.

Bedsores are also a type of necrosis. They appear in immobilized patients as a result of prolonged tissue compression or damage to the integrity of the epidermis. In this case, the formation of deep and purulent ulcerative lesions is observed.

What to do to defeat tissue necrosis? Treatment

Therapy of necrosis depends on their type. If the lesion is dry, then the tissues are treated with antiseptics, and dressings based on chlorhexidine or ethyl alcohol are applied to the place of death. The necrosis zone is dried with a five percent solution of potassium permanganate or ordinary brilliant green. Next, the affected non-viable tissues are excised, which is carried out two to three weeks after their clear designation. In this case, the incision is made in the area of viable tissue.

With dry necrosis, the underlying ailment is treated, which helps to somewhat limit the volume of dead tissues. Operational optimization of blood circulation and drug treatment are also carried out, designed to improve blood supply. Antibacterial drugs are taken to prevent secondary infection.

If the necrosis is wet, it is accompanied by the development of infection and a rather severe general intoxication, respectively, the therapy should be radical and vigorous. At an early stage of treatment, doctors try to transfer it to dry, but if such attempts do not work, the affected part of the limb is excised.

Local treatment in the treatment of wet necrosis involves washing the wound with a peroxide solution, doctors open the streaks, as well as pockets, and use different drainage techniques. In addition, the imposition of antiseptic dressings is practiced. All patients are subject to mandatory immobilization.
In parallel with local treatment, the patient is given antibiotics, detoxification solutions and vascular therapy.

At the slightest sign of necrosis, you should seek medical help.

Treatment of necrosis is local and general, while there is a fundamental difference in the treatment of dry and wet necrosis.

Dry necrosis

Local treatment carried out in two stages.

1. Prevention of infection development and tissue drying:

treatment of the skin around the necrosis with antiseptics;
dressing with ethyl alcohol, boric acid, chlorhexidine;
drying the necrosis zone with a 5% solution of potassium permanganate or an alcohol solution of brilliant green.

2. Excision of non-viable tissues - necrectomy (resection of the phalanx, amputation of the finger, foot), which is carried out after 2-3 weeks (when a demarcation line is formed) in the zone of viable tissues.

General treatment with dry necrosis, it includes the treatment of the underlying disease, i.e., the cause of necrosis, which makes it possible to limit the volume of dead tissues. Therefore, if possible, surgical restoration of blood circulation and conservative therapy, directions for improving blood supply are carried out. Antibacterial therapy is prescribed to prevent infectious complications.

Wet necrosis

A distinctive feature of wet necrosis is the development of infection and severe general intoxication, so treatment should be radical and vigorous.

In the early stages of treatment, attempts are made to convert wet necrosis to dry. If this fails, a radical necrectomy is performed - the removal of a part of the limb within healthy tissues.

Local treatment:

washing the wound with 3% hydrogen peroxide solution;
opening streaks, pockets, using different drainage methods;
bandaging with antiseptic solutions (chlorhexidine, furatsilin, boric acid);
obligatory therapeutic immobilization (gypsum splints).

General treatment:

antibacterial therapy (administration of antibiotics intravenously, intraarterially);
detoxification therapy;
vascular therapy.

Surgery: the average time allotted for the transfer of wet necrosis to dry is 1-2 days, but in each case the decision is made individually. If after a few hours conservative treatment is ineffective (inflammation progresses, the necrosis zone increases, intoxication increases), an operation is necessary - the only means of saving the patient's life. In this case, it is necessary to carry out a short-term (within 2 hours) preoperative preparation: infusion and antibiotic therapy, then operate the patient.

Surgical intervention for wet gangrene involves the removal of necrosis within intact viable tissues. Since it is known that during wet necrosis, pathogenic microbes are found in tissues located above the visible border of the inflammatory process, high amputation is performed. For example, with wet necrosis of the foot, if hyperemia and edema reach the upper third of the lower leg, amputation is done at the level of the upper third of the thigh.

General treatment is carried out according to the generally accepted scheme for the treatment of severe intoxication with purulent wounds.

V.Dmitrieva, A.Koshelev, A.Teplova

"Treatment of necrosis" and other articles from the section

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

Tissue necrosis - causes, symptoms, diagnosis and treatment

Such are the processes of slow tissue death in violation of innervation, non-healing ulcers in general exhaustion, etc.
The concept of paranecrosis is close to necrobiosis (D. N. Nasonov, V. Ya. Aleksandrov). It includes a set of features (increase in the viscosity of colloids of the cytoplasm and nucleus, a change in the electrolyte composition, an increase in the 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 are constantly taking place as a manifestation of the normal vital activity of the organism, since the administration of any function requires the expenditure of a material substrate, replenished by physiological regeneration. So, the integumentary epithelium of the skin, the epithelium of the respiratory, digestive and genitourinary tracts constantly dies and regenerates. 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 subjected to aging, "natural death" and subsequent renewal, and the lifespan of different cells is different and genetically determined. The “natural death” of a cell, which completes its aging, is followed by physiological necrosis, i.e., destruction of the cell, 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, while chromatin condensation occurs - karyopyknosis, breaks up into clumps - karyorrhexis and dissolves - karyolysis. Pyknosis, rhexis, and nuclear lysis are sequential stages of the process and reflect the dynamics of hydrolase activation - ribonuclease and deoxyribonuclease, which leads to the cleavage of phosphate groups from nucleotides and the release of nucleic acids that undergo depolymerization.
In the cytoplasm, denaturation and coagulation of proteins occur, usually replaced by colliquation, and its ultrastructures die. Changes may involve part of the cell (focal coagulative necrosis) that is rejected or the entire cell (cytoplasmic coagulation). Coagulation ends with plasmorhexis - the disintegration of the cytoplasm into clumps. At the final stage, the destruction of the membrane structures of the cell leads to its hydration, hydrolytic melting of the cytoplasm occurs - plasmolysis. Melting in some cases covers the entire cell (cytolysis), in others - only part of it (focal colliquation necrosis, or balloon degeneration). With focal necrosis, complete restoration of the outer membrane of the cell can occur. Changes in the cytoplasm (coagulation, plasmorhexis, 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. The intermediate substance swells and melts due to the depolymerization of its glycosaminoglycans and impregnation with blood plasma proteins. Collagen fibers also swell, become impregnated with plasma proteins (fibrin), turn into dense homogeneous masses, disintegrate or lyse. Changes in elastic fibers are similar to those described above: swelling, basophilia, decay, melting - elastolysis. Reticular fibers often remain in the foci of necrosis for a long time, but then they undergo fragmentation and clumpy decay; similar changes and nerve fibers. The breakdown of fibrous structures is associated with the activation of specific enzymes - collagenase and elastase. Thus, in the intercellular substance during necrosis, changes characteristic of fibrinoid necrosis most often develop. Less commonly, they are manifested by pronounced edema and mucus of the tissue, which is characteristic of colliquat necrosis. With necrosis of adipose tissue, lipolytic processes predominate. There is a splitting of neutral fats with the formation of fatty acids and soaps, which leads to reactive inflammation, 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, however, the predominance of one of them is often noted, which depends both on the cause that caused necrosis and the mechanism of its development, and on the structural features of the organ or tissue in which necrosis occurs.
With the disintegration 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, smell change. In some cases, the dead tissue becomes dense and dry (mummification), in others it becomes flabby and melts (myomalacia, encephalomalacia from Greek malakas - soft). Dead tissue is often pale and white-yellow in color. Such, for example, are foci of necrosis in the kidneys, spleen, myocardium when blood flow is stopped, foci of necrosis under the action of Mycobacterium tuberculosis. Sometimes, on the contrary, it is saturated with blood, has a dark red color. An example is the foci of circulatory necrosis in the lungs that occur against the background of venous congestion. Foci of necrosis of the skin, intestines, uterus often acquire a dirty brown, gray-green or black color, as the blood pigments that impregnate them undergo a series of changes. In some cases, foci of necrosis are stained with bile. With putrefactive fusion, dead tissue emits a characteristic bad odor.

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Types of necrosis

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

Organization of work of a nurse.

Lesson plan.

1. Reasons for the development of necrosis.

2. The 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 the organization of the work of a nurse in 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 the direct destruction of their traumatic factor or circulatory disorders.

Most often, local tissue necrosis is caused by the following factors:

1) mechanical(compression, crushing, ruptures);

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

3) electrical(a very high temperature is created at the place of exposure to a high voltage electric current);

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

5) toxic(the action 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 in a part of the body or organ as a result of prolonged spasm or obliteration of the vessel, blockage of the vessel by a thrombus or compression of the vessel by a tourniquet, tumor).

Types of necrosis

There are the following types of necrosis: heart attack; sequester; coagulation (dry) necrosis; colliquative necrosis; gangrene.

heart attack (from lat. infarcire - to stuff, stuff) - a focus of a tissue or organ that has undergone necrosis as a result of a sudden cessation of its blood supply, i.e. ischemia. Therefore, a heart attack 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 heart attack undergoes autolytic melting (resorption) followed by complete tissue regeneration. Most often, a heart attack develops according to the type of coagulative necrosis, less often - colliquational. Unfavorable outcomes of a heart attack - a violation of the vital activity of a tissue, an organ, developed complications, sometimes ending in death.

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

Journal headings

The demarcation line consists of a shaft of leukocytes and an area of granulation and connective tissue. More often, a sequester is formed in the bone with 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 sequester cavity through the fistulous passages.

Coagulation (dry) necrosis - necrosis, which develops on the basis of protein coagulation and tissue dehydration. The latter become atrophic, dry (mummified), wrinkled, dense, differently colored (mainly dark) and separated 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 exposed to hydrolytic cleavage. It can detach itself, encapsulate and organize itself, 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 colliquative necrosis with purulent-putrefactive infection and disruption of the vital activity of the tissue, organ, developed complications, sometimes ending in death.

Colliquation (wet) necrosis - necrosis, characterized by melting putrefactive microorganisms
incapable tissues. The latter become painful, edematous, tense, friable, soft, differently colored (at first pale, marbled, yellowish, then cyanotic red, at the end dirty and black, gray-green) with the presence of dark-colored foci , blisters of exfoliated epidermis (conflicts) with sanious fluid, fetid, putrid odor. Violation of the integrity of tissues, 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 tissues. The general symptoms of intoxication are expressed.

Colliquation necrosis is sometimes able to delimit and transform into coagulative necrosis or melt (dissolve) with the formation of an ulcer or cyst cavity. As a rule, wet necrosis without its elimination ends in death from a violation of the vital activity of tissues, organs, systems as a result of progressive intoxication.

Gangrene (Greek gangraina - fire) - necrosis of tissues, organs in contact with the external environment. There are gas gangrene caused by anaerobic clostridial spore-forming microorganisms, and gangrene, which is based on coagulative necrosis - dry gangrene or colliquatative necrosis - wet gangrene. These terms are more often used for necrosis of the limbs. Perhaps the development of wet gangrene of the tissues of the cheeks, perineum - noma (Greek nome - "water cancer"). Gangrene of internal organs (stomach, intestines, liver, gallbladder, pancreas, kidney, bladder, lung, etc.) is always wet. Bedsores are a type of gangrene.

Causes of necrosis

Most often lead to the development of necrosis:

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

Classification

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

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

Classification by clinical manifestations:

Colliquation necrosis (necrotic tissue changes are 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.
Sequester.
Heart attack.

Symptoms of the disease

With tuberculosis, syphilis, and some other infectious diseases, necrotic processes are characteristic of internal organs, 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 fatty tissue occur as a result of injury or exposure to enzymes of damaged glands (for example, in acute pancreatitis).

What is oral tissue necrosis?

There are several types of gangrene:

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

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

Outcome of the disease

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.

Treatment of necrosis

In most cases, drug therapy is prescribed to restore blood flow to the affected tissues or organ, if necessary, antibiotics are administered, and detoxification therapy is performed. Sometimes it is possible to help the patient only by surgery, by amputating part of the limbs or excising dead tissues.

Histological examination in the collapsing tissue reveals characteristic changes that occur both in 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 looks light due to edema ( core swelling). In apoptosis, on the contrary, there is an increase in karyopyknosis. Changes in the cell nucleus during necrosis are completed by its decay, fragmentation ( karyorrhexis). The complete destruction of the nucleus is denoted by the term karyolysis (karyolysis).

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 matrix dehydration ( coagulation of the cytoplasm), the cytoplasm is stained more intensely, while its volume decreases. With passive cell death, on the contrary, progressive edema (hydration) of the hyaloplasm and organelle matrix develops. Hydration of cytoplasmic structures of parenchymal cells in pathology is denoted by the term hydropic dystrophy, and a pronounced edema of organelles (endoplasmic reticulum, mitochondria, elements of the Golgi complex, etc.) is called "balloon dystrophy", or "focal colliquat cell necrosis". Fragmentation ("lumpy disintegration") of the cytoplasm is usually denoted by the term plasmorhexis, however, plasmorhexis 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) are depolymerized most rapidly, reticular (reticulin) fibers are destroyed the longest. Collagen fibers first increase in size due to edema, then they are liberated (divided into thinner threads) and destroyed ( collagen lysis). Elastic fibers break up into separate fragments ( elastorhexis), after which they are destroyed ( elastolysis).

DEMARCATIONAL 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 that develops around the focus of necrosis. Demarcation inflammation, like inflammation in general, provides the conditions for restoring the integrity of the damaged tissue. The main microscopic signs of inflammation are vascular plethora ( inflammatory hyperemia), edema 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. Neutrophilic granulocytes, thanks to their lysosomal enzymes and active oxygen metabolites, melt detritus and contribute to its liquefaction. The detritus thus prepared 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, foci of destruction of a small size with an adequate course of demarcation inflammation are restored completely ( full reparation – restitution), i.e. tissue similar to it regenerates in place of the damaged one. With large amounts of tissue damage, as well as with 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 reparations, or substitution, and the process of replacing detritus with fibrous connective tissue - organization. Scar tissue can undergo degenerative changes - hyalinosis and petrification(see below). Sometimes bone tissue is formed in the scar ( ossification). In addition, at the site of necrosis, for example, in the brain tissue, a cavity (cyst) may form.

The course of demarcation inflammation may be disturbed. Its most vulnerable link is the function of neutrophilic granulocytes. There are two main types pathology of demarcation inflammation: insufficient and increased activity of neutrophilic granulocytes in the lesion.

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). At the same time, part of the detritus, sometimes significant, remains in the tissue, sharply compacted due to dehydration and surrounded by scar tissue, which forms a capsule around the necrotic masses. Thus, mycobacterium tuberculosis usually inhibits the migration of neutrophilic granulocytes, therefore, in the foci of tuberculous lesions, caseous detritus is resorbed slowly and persists for a long time (persists).

2. Increased activity neutrophilic granulocytes occurs when detritus is contaminated with microorganisms, primarily pyogenic bacteria. Purulent inflammation developing in the focus of necrosis can spread to adjacent healthy tissues.

Thus, it is possible to 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 fusion) outcomes of necrosis.

Necrosis refers to the death of tissues or an entire organ. In the presence of this condition, a complete or partial metabolic disorder is noted, 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 noted, referred to in medicine paranecrosis. In the second stage, irreversible dystrophic changes on the face, which are also called necrobioses. The third stage of the development of this disease is accompanied by autolysis, that is, the decomposition of a 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 a lot of them, but a lot. First of all, these are numerous mechanical injuries.

Necrosis - description of the disease

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

We also draw the attention of all readers to the fact that this kind of tissue death in most cases occurs in fairly important organs of the human body. Most often, the heart, brain and kidneys are affected. Try to follow a healthy lifestyle in order to prevent the development of this disease. Before use, you should consult with a specialist.

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

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

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

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

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

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

Causes of the disease

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

Additional factors include:

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

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

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

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

Symptoms

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

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

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

Heat.
Chills.
Dizziness.
Nausea.

Also, when organs are affected, specific symptoms are revealed that indicate a disease of the corresponding organ. There are also pain symptoms in the infected area.

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

Types of necrosis

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

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

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

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

All important processes in the human body occur at the cellular level. Tissues, as a collection of cells, perform protective, supporting, regulatory and other significant functions. When cell metabolism is disturbed due to various reasons, destructive reactions occur that can lead to changes in the functioning of the body and even cell death. Skin necrosis is a consequence of pathological changes and can cause irreversible deadly phenomena.

What is tissue necrosis

In the human body, tissue, represented by a combination of structural and functional elementary cells and extracellular tissue structures, is involved in many vital processes. All types (epithelial, connective, nervous and muscular) interact with each other, ensuring the normal functioning of the body. The natural death of cells is an integral part of the physiological mechanism of regeneration, but the pathological processes that occur in cells and the extracellular matrix entail life-threatening changes.

The most severe consequences for living organisms are characterized by tissue necrosis - cell death under the influence of exogenous or endogenous factors. In this pathological process, swelling and a change in the native conformation of cytoplasmic protein molecules occur, which leads to the loss of their biological function. The result of necrosis is the adhesion of protein particles (flocculation) and the final destruction of the vital permanent components of the cell.

The reasons

The cessation of the vital activity of cells occurs under the influence of changed external conditions for the existence of the organism or as a result of pathological processes occurring inside it. The causative factors of necrosis are classified in terms of their exogenous and endogenous nature. Endogenous reasons why tissues can die include:

vascular- violations in the work of the cardiovascular system, which led to a violation of the blood supply to tissues, deterioration of blood circulation;
trophic- a change in the mechanism of cellular nutrition, a violation of the process of ensuring the safety of the structure and functionality of cells (for example, skin necrosis after surgery, long-term non-healing ulcers);
metabolic- a violation of metabolic processes due to the absence or insufficient production of certain enzymes, a change in the general metabolism;
allergic- a high-intensity reaction of the body to conditionally safe substances, which results in irreversible intracellular processes.

Exogenous pathogenic factors are caused by the impact on the body of external causes, such as:

mechanical- damage to the integrity of tissues (wound, trauma);
physical– violation of functionality due to the influence of physical phenomena (electric current, radiation, ionizing radiation, very high or low temperature – frostbite, burns);
chemical- Irritation by chemical compounds;
toxic- defeat by acids, alkalis, salts of heavy metals, drugs;
biological- destruction of cells under the influence of pathogenic microorganisms (bacteria, viruses, fungi) and the toxins they secrete.

signs

The onset of necrotic processes is characterized by loss of sensation in the affected area, numbness of the extremities, and a tingling sensation. The pallor of the skin indicates a deterioration in blood trophism. The cessation of the blood supply to the damaged organ leads to the fact that the skin color becomes cyanotic, and then acquires a dark green or black tint. General intoxication of the body is manifested in the deterioration of health, fatigue, exhaustion of the nervous system. The main symptoms of necrosis are:

loss of sensitivity;
numbness;
convulsions;
puffiness;
hyperemia of the skin;
sensation of coldness in the extremities;
violation of the functioning of the respiratory system (shortness of breath, changes in the rhythm of breathing);
increased heart rate;
permanent increase in body temperature.

Microscopic signs of necrosis

The branch of histology devoted to the microscopic examination of diseased tissues is called pathohistology. Specialists in this field examine sections of organs for signs of necrotic damage. The necrosis is characterized by the following changes occurring in the cells and interstitial fluid:

loss of the ability of cells to selectively stain;
core transformation;
discomplexation of cells as a result of changes in the properties of the cytoplasm;
dissolution, disintegration of an intermediate substance.

The loss of the ability of cells to stain selectively, under a microscope, looks like a pale structureless mass, without a clearly defined nucleus. The transformation of the nuclei of cells that have undergone necrotic changes develops in the following directions:

karyopyknosis- wrinkling of the cell nucleus, which occurs as a result of the activation of acid hydrolases and an increase in the concentration of chromatin (the main substance of the cell nucleus);
hyperchromatosis- there is a redistribution of chromatin clumps and their alignment along the inner shell of the nucleus;
karyorrhexis– complete rupture of the nucleus, dark blue clumps of chromatin are arranged in random order;
karyolysis- violation of the chromatin structure of the nucleus, its dissolution;
vacuolization- vesicles containing a clear liquid form in the cell nucleus.

The morphology of leukocytes has a high prognostic value in skin necrosis of infectious origin, for the study of which microscopic studies of the cytoplasm of the affected cells are carried out. Signs characterizing necrotic processes can be the following changes in the cytoplasm:

plasmolysis- melting of the cytoplasm;
plasmorhexis- the disintegration of the contents of the cell into protein clumps, when poured with xanthene dye, the studied fragment turns pink;
plasmopyknosis- wrinkling of the internal cellular environment;
hyalinization- compaction of the cytoplasm, its acquisition of uniformity, vitreousness;
plasma coagulation- as a result of denaturation and coagulation, the rigid structure of protein molecules breaks down and their natural properties are lost.

Connective tissue (intermediate substance) as a result of necrotic processes undergoes gradual dissolution, liquefaction and decay. The changes observed in histological studies occur in the following order:

mucoid swelling of collagen fibers- the fibrillar structure is erased due to the accumulation of acid mucopolysaccharides, which leads to a violation of the permeability of vascular tissue structures;
fibrinoid swelling- complete loss of fibrillar striation, atrophy of cells of the interstitial substance;
fibrinoid necrosis- splitting of the reticular and elastic fibers of the matrix, the development of structureless connective tissue.

Types of necrosis

To determine the nature of pathological changes and the appointment of appropriate treatment, it becomes necessary to classify necrosis according to several criteria. The classification is based on clinical, morphological and etiological features. In histology, several clinical and morphological varieties of necrosis are distinguished, the belonging of which to one or another group is determined based on the causes and conditions for the development of the pathology and the structural features of the tissue in which it develops:

coagulation(dry) - develops in protein-rich structures (liver, kidneys, spleen), is characterized by processes of compaction, dehydration, this type includes Zenker (waxy), adipose tissue necrosis, fibrinoid and caseous (curd-like);
colliquational(wet) - development occurs in tissues rich in moisture (brain), which undergo liquefaction due to autolytic decay;
gangrene- develops in tissues that are in contact with the external environment, there are 3 subspecies - dry, wet, gas (depending on the location);
sequestration- represents a site of a dead structure (usually a bone structure) that has not undergone self-dissolution (autolysis);
heart attack- develops as a result of an unforeseen complete or partial violation of the blood supply to the organ;
bedsores- is formed with local circulatory disorders due to constant compression.

Depending on the origin of necrotic tissue changes, the causes and conditions for their development, necrosis is classified into:

traumatic(primary and secondary) - develops under the direct influence of a pathogenic agent, according to the mechanism of occurrence, it refers to direct necrosis;
toxigenic- occurs as a result of the influence of toxins of various origins;
trophoneurotic- the cause of development is a violation of the central or peripheral nervous system, causing violations of the innervation of the skin or organs;
ischemic- occurs with insufficiency of peripheral circulation, the cause may be thrombosis, blockage of blood vessels, low oxygen content;
allergic- appears as a result of a specific reaction of the body to external stimuli, according to the mechanism of occurrence, it refers to indirect necrosis.

Exodus

The significance of the consequences of tissue necrosis for the body is determined based on the functional characteristics of the dying parts. Necrosis of the heart muscle can lead to the most severe complications. Regardless of the type of damage, the necrotic focus is a source of intoxication, to which the organs react by developing an inflammatory process (sequestration) in order to protect healthy areas from the harmful effects of toxins. The absence of a protective reaction indicates an oppressed reactivity of the immune system or a high virulence of the causative agent of necrosis.

An unfavorable outcome is characterized by purulent fusion of damaged cells, a complication of which is sepsis and bleeding. Necrotic changes in vital organs (cortical layer of the kidneys, pancreas, spleen, brain) can be fatal. With a favorable outcome, the dead cells melt under the influence of enzymes and the dead areas are replaced with an interstitial substance, which can occur in the following directions:

organization- the place of necrotic tissue is replaced by connective tissue with the formation of scars;
ossification- the dead area is replaced by bone tissue;
encapsulation- a connecting capsule is formed around the necrotic focus;
mutilation- the outer parts of the body are rejected, self-amputation of dead areas occurs;
petrification- calcification of areas subjected to necrosis (replacement with calcium salts).

Diagnostics

It is not difficult for a histologist to identify necrotic changes of a superficial nature. To confirm the diagnosis, based on oral questioning of the patient and visual examination, testing of blood and a sample of fluid from the injured surface will be required. If there is suspicion of the formation of gases with diagnosed gangrene, an x-ray will be prescribed. The necrosis of tissues of internal organs requires a more thorough and extensive diagnosis, which includes methods such as:

X-ray examination- is used as a method of differential diagnosis to exclude the possibility of other diseases with similar symptoms, the method is effective in the early stages of the disease;
radioisotope scanning- shown in the absence of convincing X-ray results, the essence of the procedure is the introduction of a special solution containing radioactive substances, which are clearly visible in the image during the scan, while the affected tissues, due to impaired blood circulation, will be clearly distinguished;
CT scan- it is carried out with suspicion of the death of bone tissue, during the diagnosis, cystic cavities are detected, the presence of fluid in which indicates a pathology;
Magnetic resonance imaging is a highly effective and safe method for diagnosing all stages and forms of necrosis, with the help of which even insignificant cell changes are detected.

Treatment

When prescribing therapeutic measures for diagnosed tissue death, a number of important points are taken into account, such as the form and type of the disease, the stage of necrosis and the presence of concomitant diseases. The general treatment of soft tissue skin necrosis involves the use of pharmacological drugs to maintain the body depleted by the disease and strengthen the immune system. For this purpose, the following types of drugs are prescribed:

antibacterial agents;
sorbents;
enzyme preparations;
diuretics;
vitamin complexes;
vasodilators.

Specific treatment of superficial necrotic lesions depends on the form of pathology:

Purpose of therapyMethods of treatment Wet

With the localization of necrotic lesions in the internal organs, treatment consists in applying a wide range of measures to minimize pain symptoms and preserve the integrity of vital organs. The complex of therapeutic measures includes:

drug therapy - taking non-steroidal anti-inflammatory drugs, vasodilators, chondroprotectors, drugs that help restore bone tissue (vitamin D, calcitonitis);
hirudotherapy (treatment with medicinal leeches);
manual therapy (according to indications);
therapeutic physical exercises;
physiotherapeutic procedures (laser therapy, mud therapy, ozokerite therapy);
surgical methods of treatment.

Surgical intervention

Surgical impact on the affected surfaces is used only if the conservative treatment is ineffective. The decision on the need for an operation should be made immediately if there are no positive results of the measures taken for more than 2 days. Delay without good reason can lead to life-threatening complications. Depending on the stage and type of the disease, one of the following procedures is prescribed:

Type of surgical intervention	Indications for the operation	The essence of the procedure	Possible Complications
Necrotomy	Early stages of the development of the disease, wet gangrene with localization in the chest or extremities	Apply striped or cellular incisions of dead integument and adjacent tissues before the onset of bleeding. The purpose of the manipulation is to reduce the intoxication of the body by removing the accumulated fluid.	Rarely, infection at the incision site
Necrotomy	Wet necrosis, the appearance of a visible demarcation zone separating viable tissue from dead tissue	Removal of necrotic areas within the affected area	Infection, divergence of superimposed sutures
Amputation	Progressive wet necrosis (gangrene), no positive changes after conservative therapy	Truncation of a limb, organ or soft integument by resection significantly higher than the visually determined affected area	Death of tissues on the part of the limb remaining after resection, angiotrophoneurosis, phantom pain
Endoprosthetics	Bone lesions	A complex of complex surgical procedures for the replacement of affected joints with prostheses made of high-strength materials	Infection, displacement of the installed prosthesis
Artrodes	The death of bone tissue	Resection of bones with their subsequent articulation and fusion	Decreased patient's ability to work, limited mobility

Preventive measures

Knowing the fundamental risk factors for the occurrence of necrotic processes, preventive measures should be taken to prevent the development of pathology. Along with the recommended measures, it is necessary to regularly diagnose the state of organs and systems, and if suspicious signs are found, seek advice from a specialist. Prevention of pathological cellular changes is:

reducing the risk of injury;
strengthening the vascular system;
increase the body's defenses;
timely treatment of infectious diseases, acute respiratory viral infection (ARVI), chronic diseases.

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Attention! The information presented in the article is for informational purposes only. The materials of the article do not call for self-treatment. Only a qualified doctor can make a diagnosis and give recommendations for treatment based on the individual characteristics of a particular patient.

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