2. Local:

• Features of structure of the vascular system (magistral or ramose)

• A state of a vascular wall (sclerosis, inflammation)

• A degree of development of vascular collaterals in the area of the affection

• Correlation of speed of development of violation of circulation of blood and switching on compensatory mechanisms

• A degree of differentiation of tissues and viscera, activity of metabolism, tension of enzyme processes, functional stress, firmness to a hypoxia

• A degree of a microbial semination

• A level of hydration of tissues content of albumens

3. Character, strength, duration of an action of a pathogenic factor

• Intensity of formation of toxins a microflora;

• Physical conditions: action of low temperatures (draws a disorder of circulation of blood), surplus warming (increase of intensity of metabolism in the conditions of insufficiency of circulation of blood), penetrable radiation.

4. Mechanism of development of necrosis:

• direct;

• indirect

Concrete correlation of these factors is predetermined to an origin dry (coagulative) or colliquative necrosis.

Microscopic signs of a necrosis.

Changes of the cell nucleus: shrinkage (caryopicnosis), lysis (caryolysis) or disintegration.

Changes of the cytoplasm: denaturation and coagulation of albumens, death of ultrastructures, disintegration on blocks (plasmorexis), hydrolysis dissolution (plasmolylis).

Changes of intercellular space:

• An intermediate substance swells and is dissolved

• Collagen fibres swell, are saturated with plasma albumens (fibrin), change into dense| homogeneous masses and are disintegrated or lysed.

• Elastic fibres swell, disintegrate, are melted (elastolis)

• Textiform fibres are fragmented, disintegrate on blocks

• Nervous fibres – like.

Fibrinoid degeneration is completion of the fibrinoid swelling and characterized total destruction of connective tissue. Usually there is the expressed reaction of macrophages, increase of permeability of a vascular wall, formation of a fibrinoid (this substance consists an albumen, polysaccharides of disintegrated fibres; an obligatory component is a fibrin).

Results of necrosis:

1. Resolution

2. Rejection

3. Organization is a substitution connective tissue (scar)

4. Encapsulation is becoming overgrown with connective tissue and formation of a capsule.

5. Ossification is formation of bone tissue in the area of the necrosis

6. Petrification

7. Formation of a cyst is a limiting to the capsule from connective tissue of the cavity which appears at resolution of the tissue detritus.

8. Purulent dissolution of a focus of a necrosis.

Clinic of necrosis

It depends from:

1. Localization (superficial, deep) is a brightness of visual changes

2. Prevalence is an area displays of a necrosis are presented on

3. Functional condition of the staggered organ (areas) causes the proper functional disorders

4. The type of a necrosis causes local and general symptomatology.

Local symptomatology includes:

• Direct signs are discolorations, closeness and elasticity of tissues, decreasing of the temperature of the skin, disorders of motions and sensitiveness

• Indirect signs are reactive changes round the located formations, for example signs of peritonitis at a gangrene of the intestine owing to thrombosis mesenteric vessels or putrid empyema of pleura at the gangrene of a lung.

General symptomatology is intoxication and polyorgan insufficiency.

Diagnostics at presence of necrosis:

1. Estimation of symptoms: local signs, signs of parafunction organs.

2. Exposure of possible reason main disease on the basis of physical investigation and additional methods.

General principles of treatment of a necrosis

1. Treatment of a reason disease

2. Necretomy (amputation, exarticulation, resection).

3. Improvement of the general condition of organism: detoxication, therapy by antibiotics, immunocorection, support of function of life-support organs and systems.

Prophylaxis:

1. warning, early diagnostics and treatment of diseases which draw necrosis;

2. proceeding in disorders of circulation of blood (liquidation of spasm of vessels, stimulation of opening of collaterals – is novocaine blockades, spasmolytics, by-passing and prosthetics of vessels, tromb- and embolectomy, intravenous infusion of fibrinolitics);

3. at violation of circulation of blood for limitation of necrosis or warnings of his development – measures on the improvement of trophism or diminishing of intensity of metabolism in them: rest, novocaine blockades for liquidation of reflex spasm of collaterals.

Separated types of necrosis

Dry gangrene (mummification). Gangrene in a word for word a translation from a Greek is a fire.

Etiology and pathogeny. Slowly making progress violations of circulation of blood, for the exhausted, water-free patients, in tissues rich on albumens and on a liquid results poor in development of coagulate necrosis, which denaturizing of albumen is underpaid with formation of insoluble connections which long time can be not added the hydrolysis breaking up. Rotting are thus dehydrated and does not test|.

A gangrene is begun with the peripheral departments of extremities, spreads proximal to the level of sufficient collateral circulation of blood. Here a demarcation billow develops on verge of dead and viable tissues. It is an area of development of reactive inflammation which limits dead tissues. In this area blood vessels are extended, arise up hyperaemia, was swollen, plenty of leucocytes which select hydrolyses is saved. A demarcation billow prevent considerable suction of toxins and endotoxicosis does not develop.

A blood pigment impregnates with dead tissues and forms their characteristic colouring (umber, grey-yellow, black).

A microflora in this case develops badly. But, in an initial period active development of putrid flora and passing is possible to the moist gangrene.

Clinical signs

Complaints – at the beginning great ischemic pain is possible below than place of occlusion of an artery, paresthesia.

Objectively – a skin is cyanotic, it is marble and cold. A pulse on peripheral arteries is not determined. Gipo-(rarer anaesthesia). Disorders of function of extremity. Motions can be stored. Tissues are dry, mummified, dense, umber, grey-yellow, black with a blue tint. General symptoms |as a rule is absent or poorly expressed.

clinical course

Necrotizing changes do not make progress usually. Tearing away of necrotizing tissues is possible long after. In an initial period active development of putrid flora and passing is possible to the moist gangrene.

TREATMENT. Necrectomy or amputation after complete and clear appearance of demarcation. To it is a torrefaction of necrotizing tissues (spirit compresses, sorbents). For warning of progress of necrotizing changes (improvement of trophism of tissues) and prophylaxis of infection (aseptic bandage, antibiotics).

Moist (putrid) gangrene. Moist (colliquative) necrosis.

Etiology and pathogeny. Develops at rapid violation of circulation of blood (embolism, trauma of vessel and etc). Favourable conditions – a fatty cellulose, low maintenance of albumen and far of water in tissues is expressed (that terms, friendly to the hydrolysis).

The thrombosis of main veins of lower extremities at an undeveloped collateral net and maintenance of arterial circulation also conduces to development of moist gangrene/

A moist gangrene is observed at necrosis of internal (intestine, lights, gall-bladder, appendix) which exist in the conditions of sufficient hydratation. It is an always moist gangrene. Present terms (nourishing environment, stationary temperature, oppressing of the immune system) are instrumental in the vital functions of microflora which actively participates in development of process (bacteroids, proteus).

The origin of the second necrosis conduces to rapid progress a disease and hinders| development of demarcation billow.

Dead tissues do not have time to dry out, have moist disintegration. It conduces to suction of products of disintegration of tisssues and microbal toxins, development of endotoxicosis, sepsis. There is the real threat life of patient.

clinical course

Complaints about pain in the staggered area. Natively – the oedema of lower extremities, pallor of skin, grows sharply. Skin – marble, cold. Appearance of visible net of bluish saphena, crimson spots, bubbles is possible (gap-filling). A pulse is not determined. Motions are absent. At disintegration tissues grow into stinking grey-green mass.

The gangrene of organs of abdominal region shows up the clinic of peritonitis. At a gangrene lights plenty of stinking foamy sputum.

General symptoms are symptoms of endotoxicosis and signs of functional insufficiency of vital (grave general condition, dry tongue, psychosis, languor, dormancy, tachycardia, hypotension, oliguria, shortness of breath, hyperthermia, anaemia, leucocytosis with a neutrophylosis.

There is rapid progress of necrotizing changes, endotoxicosis, sepsis. Especially heavy course is for patients with diabetes mellitus.

TREATMENT. A basic element is early amputation (delete of the changed organ or its part) with the purpose of rescue life. Amputation needs to be conducted on sufficient distance from the visual border of dead and viable tissues, that allows to avoid development of second necrosis and subsequent progress of gangrene. For example, at the gangrene of foot on soil of diabetic angiopathy at presence of regional lymphadenitis, intoxication, development of sepsis, amputation at the level of the middle third of thigh is indicated. At the gangrene of intestine from the higher mentioned border 30-40 sm to proximal, distal – 15 – 20 sm.

Necessarily perform detoxication, antibacterial therapy, correction of functional violations of vital organs, immunotherapy.

ULCERS

An ulcer (В) is a defect integumentary and deeper located tissues which develops as a result of tearing away of necrotic tissues. Characterized a chronic course, absence or poorly expressed regeneration and resistance to the medical measures.

Reasons – look „Necrosis” and "Violations of regional hemodynamics".

On a background a devascularization of tissues (venous hypertensions and disorders of blood circulation, aterovenous anastomoses, hypoxia, acidosis), innervation, trophism. Starting factor insignificant traumas (microtraumas), protracted compression, microbial factor, autoimmune processes and allergy, can act part (the albumens of organism are acquired by АG-properties, auto-AG are produced, bars appear immune complexes which block systems of T- and V-lymphocytes and draw a local immunological reaction as infiltration leucocytes and plasmocytes of perivasallic tisssues, a local allergic reaction matters on medicines). At part| of patients setting reason is not succeeded. Contributory infringement and supporting factors are anemia, diabetes, hypoproteinemia.