NECROSIS. GANGRENE

NECROSIS

Necrosis is a local mortification of the tissue. The reason for local mortification of the tissue can be direct damage to tissue by any traumatic factor, insufficient nutrition of the tissue as a result of infringement of blood circulation, metabolic diseases, damage to the nervous system.

External factors, which injure tissues, can be the following:

mechanical factors (blows, compression, ruptures, wounds, etc.);

thermal factors (burns and frostbite);

electric factors (electrotrauma);

chemical factors (concentrated acids and alkalis, other caustics and organ secretions);

toxic factors (microbic toxins);

radiation energy (burns by X-ray radiation and radioactive burns).

Nutrition insufficiency of tissue can cause such infringements of blood circulation:

acute cardiac failure;

embolism of vessels;

long spasms or obliteration of blood vessels (Raynaud’s disease, Buerger’s disease, obliterating endarteritis, obliterating atherosclerosis, nonspecific aortoarteritis);

rupture and compression of vessels (wound to the main vessels, their compression while squeezing in the hernial gates or any type of strangulated intestinal obstruction, compression by hard plaster bandages or long-term tourniquet application);

infringement of the coagulation system of blood by hypercoagulation and rheological properties of the blood;

infringement of the integrity and structure of the intima of the blood vessels (thromboses and inflammations of the arterial and venous walls, atherosclerosis).

Insufficiency of tissue nutrition can be observed with metabolic diseases, for example, diabetes, scorbutus. Infringements of tissue nutrition and trophics are observed with damage to the nervous system (tumor, neurosyphilis, syringomyelia), and also with damages to the head and spinal cord and peripheral nerves.

In the occurrence, development and progress of necrosis big role is played both by the general anatomic and physiological features of an organism and local ones. The degree of the organism’s reactance, hypovitaminosis, and accompanying diseases belong to general features of an organism. The local ones include the structure type of the vascular system (main or collateral), type of development of infringements of blood circulation, presence of pathological changes in the vessels, presence of microbes and their toxins at the necrosis area.

Necroses can develop in different organs and tissues; they are classified by their aetiology, depth of injury and the clinical course:

according to aetiology — specific and nonspecific;

according to the depth of the damaged tissue — superficial, deep, total;

according to the clinical course — dry, humid.

Nonspecific necrosis is the result of wounds or long compression of blood vessels and tissues, extensive burns, surgical infection, trophic changes (bed sores, ulcers), thromboses and embolisms. Specific necrosis is the result of atherosclerosis, obliterating endarteritis, syphilis, endocrinal pathologies (diabetes).

Necrosis can be coagulational (dry), as observed with burns by concentrated acids, and liquefactive (humid), observed with radiation burns. Obvious attributes of necrosis arise 4–6 h after the tissue dies. Dead tissue, under the influence of proteolytic enzymes rejects. If the necrotic masses are located on the body surface after rejection, an ulcer is formed. With extensive and deep necrosis, tissue disintegration and diffusion of toxic products can lead to acutely pronounced intoxication, the development of toxic shock and the death of the patient.

GANGRENE

Gangrene is one of the forms of necrosis, predetermined by infringement of blood circulation and the development of dead tissue. The most often reason for the development of gangrene is acute or chronic arterial insufficiency. Dry, or coagulative, and humid gangrene are distinguished.

Dry Gangrene

Dry gangrene affects the extremities more often. It is characterized by fast drying of dead tissue without infection and it appears mummification of dead tissue. The tissue quickly becomes dehydrated and dries up, turning brown or blue-black.

The necrosis process is limited and usually does not progress. Histologically in the tissue coagulative necrosis with the disintegration of the cellular nucleus, erythrocytes, leukocytes and settlement of protein in the plasma is marked. Clinically in the initial stage, strong ischemic pains in the extremities more distal from the damage, as a rule, are observed. The extremity becomes pale and is cold to the touch; the skin gradually gets a marble look.

Superficial and deep sensitivity becomes dull and then completely disappears; the function of the extremities is broken. Pulse on the peripheral arteries is not determined. If at the same time with occlusion of the main vessel there is resistant spasm of the collaterals, the necrosis zone becomes more extensive. Further a demarcation shaft, which limits the living tissue from the dead ones, develops. The dead tissue comes off, and at the demarcation line the connective tissue cells multiple, the leukocytes accumulate and granulations form. The border between the alive and dead tissue goes deeper, untill the necrotic area rejects, after which there is a granulating wound, which slowly heals. As a result of the mummification of dead tissue during dry gangrene, absorption of toxic substances of tissue disintegration is not significant and intoxication does not occur. The general condition of the patient is good. In order to prevent the occurrence of local complications, the infection of dead tissue and the transition of dry gangrene into humid during redressing, it is necessary to strictly follow the rules of aseptics. The extremity is immobilized, dry bandages are applied, physiotherapeutic procedures (quartz irradiation) are conducted. Necrectomy, i.e. surgical removal of necrotic tissue, as well as amputation of the extremity is necessary to postpone until the occurrence of a demarcation shaft is in full view. If gangrene is caused by direct damage of tissue, necrectomy is necessary to conduct behind the demarcation line. If gangrene developed as a result of infringement of arterial blood circulation, the amputation of the extremity is conducted considerably more proximal, i.e. within the borders of absolutely viable tissue with good blood supply. In order to prevent the development of dry gangrene, early diagnosis and treatment of blood vessels diseases, which can lead to the development of necrosis and gangrene (thromboses, obliterating endarteritis and atherosclerosis) have crucial importance. It is necessary to improve blood circulation, promote the development of collaterals, and liquidate the spasm of blood vessels. It is necessary to conduct in due time reconstructive operations on vessels to normalize the blood supply of the extremities.

Humid gangrene

Humid gangrene is also a kind of necrosis. It develops mainly in obese, pastous patients as a result of acute infringement of blood circulation. Purulent or putrefactive infection frequently accompanies humid gangrene. The development of humid gangrene is also promoted by hypostases, which results from cardiac failure, renal diseases and diabetes.

With humid gangrene, the dead tissue does not dry up and become a good nutrient medium for infection. Putrefactive (protruding) disintegration of tissue develops, which is quite often accompanied by anaerobic infection (gas gangrene).

When the dead tissue breaks up, it turns into a wet dirty mass of grayish-green color with an unpleasant odour. Intensive absorption of the disintegration products, which quickly results in severe intoxication leading to the death of the patient, is observed. With humid gangrene the demarcation line is not formed, the process spreads quickly to the external tissue. The extremities become pale, cold to the touch and then cyanotic-red dots appear; the epidermis exfoliates and blisters, filled with bloody, stinking exudate, form; hypostasis of tissue sharply increases. Severe pain occurs in the damaged extremity. The mentioned above local phenomena are accompanied by systematic intoxication. The patient’s face becomes grey; tongue is dry; pulse is of weak filling and pressure; the arterial pressure is low, complete apathy and high temperature of hectic origin is observed.

The course of diabetic gangrene is especially severe. Patients with diabetes have decreased resistancy and tissue regenerative properties and increased susceptibility of an organism to pathogenic organisms of pyo-septic infection. Because of this, patients with diabetes easily get secondary inflammations, and the wounds regenerate very badly. Humid gangrene can damage different organs and as a result the clinical picture is diverse. It depends upon the type of tissue, the character and localization of the damaged organ. Gangrene of internal organs occurs only as humid gangrene and is accompanied by symptoms of peritoneal irritation and peritonitis development. Pulmonary gangrene has its own clinical signs.

The treatment for humid gangrene is directed on fast elimination of damaged cells, struggle against intoxication and infection, correction of metabolism infringement.

Necrectomy with humid gangrene is not effective because it does not improve the patient’s condition, does not liquidate the source of intoxication. With gangrene of the abdominal organs, emergency laparotomy, the removal of the damaged organ and sanitation of the abdominal cavity, is done. Broad-spectrum antibiotics, sulfamidin and nitrofuran preparations, antiseptics, vaccines and serum, immunomodulators are applied to struggle against infection. For struggle against intoxication all the available methods of intra- and extracorporal detoxification are used: introduction of great amount of crystalloids (isotonic solution of sodium chloride, 5–10% solution of glucose), haemotransfusion, plasma, albumin, haemodesum and other blood substitutes, lactosol, low-molecular polyglucin in combination with cardiac and diuretic substances (technique of forced diuresis). It is necessary to apply also haemosorption, plasmosorption, ultra-violet irradiation of blood (UVIB). Along with the therapist-endocrinologist, correction of the carbohydrate metabolism disorders are conducted for patients with diabetes.

DECUBITUS

Decubitus is a version of necrosis. This is dystrophic, ulcer-necrotic changes on the skin, fatty hypodermis and soft tissue down to the bones, which develop as a result of infringement of microcirculation caused by compression.

Compression occurs on areas of the coccygeal bone, scapula, heals, etc. Decubitus occurs in weakened patients, especially with damages to the spinal cord, in the postoperative period when patients are immobile in bed for a long time. Decubitus forms gradually, imperceptibly. First, the patients complain of feeling of compression and pain. The first attributes of decubitus is pale skin with redness following. Then it is joined by cyanosis; hypostasis develops; the epidermis exfoliates; blisters, filled with serous-hemorrhagic exudate, form. Soft tissue dies down to the periosteum. The skin dies; necrotic tissue separates and forms a deep purulent wound, the bottom which is the periosteum of the next bone. An infection can lead to the development of sepsis and the patient’s death.

Preventive measures against decubitus have crucial importance. Such patients should be turned over every 2 h and left in that position for some minutes. It is necessary to watch and change regularly bed linen and underwear; there should be no wrinkles in the bed linen. It is necessary to re-make the bed 2–3 times a day. It is necessary to watch daily the cleanliness of the integuments, wash areas where decubitus form often with warm water, then wipe it with a tampon moistened in a 10% solution of camphor spirit, with rotary movements rub and massage them. The skin on the maceration sites should be washed with cold water and soap, diligently dried, wiped with spirit and powdered. Under the pelvis and sacrum they put a rubber circle covered with a film, and under heals and elbows — cotton-gauze circles. Seriously ill patients are put on special porolon or mattresses, which are filled with water or air.

Sometimes in the medical practice it is possible to observe a socalled internal decubitus, for example, dead vein walls as a result of the presence of dense catheter in it for a long time for intravenous introduction of medicines or dead internal organ body walls, which underwent compression by a dense drainage tube. Preventive measures for the above-stated internal decubitus consists in that dense catheters and drainage tubes shouldn’t remain in patient’s organs for a long time.

It is much more difficult to treat decubitus, which formed, than prevent its formation. Decubitus are treated with a concentrated solution of potassium permanganate, powder with streptocide and rubbed with brilliant green or water solution of methylene blue. The surface of the decubitus should be covered with aseptic bandage and a 10% streptocide ointment or a 1% streptocide emulsion. It is necessary to apply physiotherapy (UV-rays, quartz). When necrosis is restricted, the line of demarcation forms; the dead tissue is surgically removed, i.e. necrotomy is conducted, or they are melted with proteolytic enzymes (trypsin, chymotrypsin). This treatment is joined with applying bandages with hypertonic solutions (10% solution of sodium chloride). After cleansing the wound, various ointment bandages are used with antiseptics, stimulating therapy (hemotransfusion, plasma, protein blood substitutes), and if necessary — surgical treatment — skin transplantation (autodermoplastic).

ULCERS

Ulcer is a defect of the skin or mucous membrane, formed as a result of necrosis tissue. After the dead tissue rejection, the defect takes a long time to heal, which results in the formation of an ulcer. The principal cause of ulcers is a sharp decrease in regeneration processes, predetermined by the general condition of the patient or the accompanying diseases or metabolism illnesses. Tissue anemia and trophic changes in tissue play an important role in their formation.

The reasons for ulcers are the following:

Infringement of arterial blood circulation (thromboses, embolism, severe angiospasm), venous blood circulation (varicose dilation, superficial and deep thrombophlebitis, arteriovenous fistulas), as well as lymph circulation disorders.

Changes in the vessel walls during atherosclerosis, obliteratingendarteritis, the Raynaud’s disease, and syphilitic aortitis.

Traumatic damages of various genesis — mechanical, thermal, chemical, electric, radiation.

Infections — purulent, putrefactive, specific (tuberculosis, syphilis, leprosy) and mycotic (actinomycosis, blastomycosis, epidermomycosis).

Disorders of metabolism processes (diabetes, scurvy, blood diseases, anemia).

Neurotrophic disorders (with traumatic damages and radicular tumours of the spinal and peripheral nerves, syringomyelia and progressive paralysis).

Benign and malignant tumours, which are inclined to be coveredby ulcers (sarcoma, lymphogranulomatosis).

First, necrotic cells with dead tissue, microbes are formed with purulent discharge. Around this cell, a granulation shaft develops, which changes into dense connective tissue, and around the ulcer nonspecific inflammation is observed. The formation of an ulcer occurs against a background of signs of pronounced trophic infringement. Its appearance and sizes can be diverse, the form — from round or extended to any shape. The edges of the ulcer can be both smooth and even or uneven, jagged, pale or cyanotic. The bottom of the ulcer usually is raised or crateriform, filled with a muddy liquid, granulation tissue and necrotic cells. Ulcers, which border a dense layer of connective tissue, are called callous ulcers. Ulcers can sometimes be covered by fungoid hypergranulations.

Ulcers can cause different complications, for example: secondary bleeding from erosive blood vessels, accompanied by infection, penetration, i.e. germination of an ulcer into adjoining organs, or perforation of an ulcer into the cavity or a neighboring hollow organ. With the healing of extensive ulcers, scars can form, which deform the organ and break its function. Malignant regeneration, a so-called malignancy of ulcers, which sharply change the clinical displays, medical policy and the prognosis of each individual case, is possible. Healed ulcers are inclined to recur.

Treatment of ulcers should be complex, directed on the elimination of the basic disease, i.e. etiologically directed. Conservative means are applied more often for treatment of external ulcers: bed regimen, immobilization of the extremity in the raised position, careful skin care, physiotherapeutic actions (ultra-violet irradiation). It is necessary to follow all aseptic rules. In the initial stage, bandages with hypertonic solutions are applied on the ulcer; proteolytic enzymes are used for complete cleansing of the ulcer from pyo-necrotic mass and infection. After the ulcer is cleansed, bandages with ointments and antiseptics are applied. Hypergranulations are cauterized with a 10% solution of silver nitrate (argentum nitricum); delete with the help of a sharp Volkmann’s curette; the extremity is immobilized with a zinc-gelatinous bandage, consisting of zinc-gelatinous glue and bandage. Zinc-gelatinous glue contains 3 parts of zinc oxide and 3 parts of gelatin, 5 parts of glycerin and 9 parts of water. Before the usage, the mixture is warmed, put on the extremity, and dressed with a soft bandage.

Besides of local treatment of ulcers, it is necessary to conduct general therapy, directed on the stimulation of immune-biological and reparation processes in an organism. With this purpose they apply full-volume, rich in vitamins meal, immunomodulating factors, protein preparations and blood substitutes, physiotherapy exercises, etc.

When conservative actions fail, they apply operative methods of treatment, which provide the cleansing of an ulcer from pathologically changed granulations and circular scars. If the tissue defect is formed, it is covered with a skin transplant or regional skin grafting on a wide pedicle is conducted.

Atherosclerotic ulcers arise in aged persons. They are mostly located in the lower third of the shin and on the feet. They are small, round or oval. The granulations are languid, pale; the edges of the ulcer are flat, dense, and uneven. Pronounced signs of chronic arterial insufficiency are observed.

Varicose-trophic ulcers are big and more often located on the internal area of the bone. The ulcers are usually deep, the neighboring tissue is dense and sclerotic, the skin has dark spots, during palpation — not very painful. Ulcers are always incorporated with varicose dilation of superficial veins on the legs, which are the basic diagnostic attributes for the formation of ulcers. Ulcers which appear against a background of chronic venous insufficiency after thrombophlebitis of deep veins on the legs, are called post-thrombophlebitic. They can be of huge sizes, located on the internal surface of the shin or circular as a cuff surrounding the whole shin. The skin of the shin around the ulcer is pigmented, swollen, dense, acute sclerotic (indurative cellulitis).

For treatment of varicose-trophic ulcers — their faster cleansing and closing — along with hypertonic and proteolytic enzymes, vacuuming with the help of special vacuum-devices, as well as treatments in special aerotherapeutic installations (ATI) have been successfully used in our clinic. Treatment of ulcers in ATI occurs under certain conditions — temperature, humidity and sterile air, which pass through special antibacterial filters.

With varicose-trophic ulcers after their closing, surgical treatment is necessary — removal of the delated superficial veins and suturing the perforated veins, normalizing venous circulation in the legs. If it is impossible to conduct surgical treatment, the varicose nodes are thrombosed by entering phlebosclerotic substances (66% solution of glucose, varicocidum).

Radiation ulcers result from the action of ionizing irradiation — during radiation therapy or casual irradiation. The formation of necrosis is preceded by changes on the skin — pigmentation, bright red teleangiectasia, hair loss, atrophy. Then necrosis with the formation of a trophic ulcer, occurring deep with a round or oval form and twisting edges, occurs. Around the ulcer, the zone of sclerotic hypodermis and atrophied skin is found. If the ulcers cover a tumour, a dense infiltrate, which enters the depth, is found, is not displaced during palpation, soldered with the surrounding tissues and organs, where the ulcer is located. The ulcer is thickened, dense, tuberous, uneven edges; the bottom is covered with necrotic tissue; sites of growths on the edges of the ulcer, which testify to the continuing active growth of the tumour, are frequently observed. With suspicion of malignancy, i.e. malignant regeneration of the ulcer, it is necessary to conduct a biopsy — incision of the edge of the ulcer for following histologic exam, that will determine subsequent medical policy.

For effective treatment, it is necessary to know and take into account the ulcer formation pathogenesis. Treatment should be pathogenetic, i.e. directed on the trophic normalization of tissue and the basic pathological processes, which entails the ulcer formation. Fortifying therapy also has great value in the complex treatment of ulcers: vitamin therapy, full-value nutrition, the use of anabolics and normalization of metabolism processes. For fixing a positive effect in the patient, it is necessary to recommend sanatorium treatment. The use of hydrosulphuric, radonic mineral baths, and mud baths improves the tissue trophic and normalizes blood and lymph circulation, which is effective preventive measures of ulcer relapses.

FISTULA

Fistula is an abnormal pathological duct in tissues, a narrow channel covered with epithelium or granulations, and which connects an organ, a natural or pathological cavity with the organ’s surface or with each other. If the channel connects a hollow organ or whith any cavity with the superficial covers, it is an external fistula. If the pathological duct connects hollow organs, it is an inner fistula. The latter should be distinguished from anastomosis, applied artificially with medical purpose.

Fistulae are divided into congenital, resulting from infringement of embryogenesis (defects of development), and acquired, resulting from trauma, tumours, inflammatory diseases. Fistulae are also a result of operative intervention which ended with the artificial formation of an external fistula and is an intermediate or final stage of the surgical treatment. For example, imposing gastrostomy, enteroand colostomy, cystostomy.

After the structure fistulae are divided into tubular, the walls of which are covered with granulations, and labia-shaped  — the walls are covered with epithelium. Tubular, or granulating, fistulae are covered with granulation tissue from the inside along the whole length of the channel; they have a tendency to close independently. Labia-shaped, or epitheliated, fistulae are covered with epithelium, which directly pass into the epidermis of the surrounding integument. Such fistulae are not inclined to close independently and require surgical treatment.

Fistulae are also distinguished according to the type of discharge: mucous, purulent, uric, biliary, feces, salivary, liquor. In the fistula’s secretion pathological elements, which help determine the diagnosis (microbacteria tuberculosis, actinomycosis, bone sequestrations, malignant cells) can be found. The secretion from the fistula, getting on the skin, can cause its irritation, maceration and formation of ulcers, observed with duodenal, small intestinal and pancreatic fistulae.

Every external fistula has external skin orifice, channel and an internal orifice. Some fistulae have no channel, because the wall of the organ can reach the level of the skin or even to stick above it, forming a lip.

Labia-shaped fistulae can be complete if the contents of the organ, for example the intestines, discharges outside, and incomplete if the contents of the organ only partly discharge through the fistula opening. For the development of labia-shaped fistula and its functioning, the eperon, which forms as a result of the posterior back wall of the intestine falling into the opening of the fistula, has crucial importance. The length of the fistula duct depends upon the thickness of the tissue through which the fistula passes, mobility of the organ, its displacement by the pathological process, presence of accretions between organs. The skin orifice of the external fistula can be of various size and form. Most often external fistulae are single, but may be plural. The formation mechanism of plural fistulae is the following: near the already existing single fistula numerous paths containing the pus, which results in the formation of multiple abscesses, which then break to the outside and form plural fistula. Actinomycosis is a disease where primarily-plural fistulae are more often formed.

The fistula clinical course consists of local and general symptoms. Local symptoms are the presence of the fistula, its localization, character of discharge, skin maceration around the external orifice, structure of the channel. General symptoms are those of the basic disease which is the reason for fistula, such as trauma, defects of development, illness.

A patient with a fistula is examined by the general plan: complaints of the patient on the presence of the fistula, character and amount of discharge, dependence on meal, defecation and urination. It is necessary to take into account anamnestic data — the fistula occurrence time (congenital or acquired) and reason for its occurrence (trauma or result of an operation). It is necessary to examine carefully the fistula, find its localization, structure (tubular or labia-shaped), type and amount of discharge. Laboratory and instrumental study of the fistula is conducted. It is necessary to use color indicators to establish the diagnosis. The patient is given a solution of dye to drink, for example, methylene blue, and the time of its appearence in the fistula should be marked. This method of diagnosis helps to determine the height of the fistula, which is especially important with a fistula of the esophagus, stomach, and duodenum.

While examining a patient with a fistula, “X-ray” methods — fistulography — are important. The liquid contrast substance is entered to the fistula through a thin catheter; the X-ray pictures are taken. On the roentgenograms they determine the localization and direction of the fistula path, presence of discharge, detect the organ that the fistula, its level, and possible pathological changes in its wall.

With the suspicion of the inner fistula, i.e. fistula of the internal organs, it is necessary to conduct radiopaque study of the esophagus, stomach, small and large intestines. With this purpose, barium or the other radiopaque substance is entered into the organ cavity and its overflow through the organ’s wall into the surrounding tissue, cavities or outside is determined.

Today for diagnosis of fistulae, specification of their localization, and sizes, endoscopic methods of study, such as gastroscopy, colonoscopy, bronchoscopy, cystoscopy, etc., based on the usage of fiber optics and optical paths, are widely used. Endoscopes may be entered through natural apertures inside any hollow organ and to carefully examine its wall. In some cases, an inner fistula can be found during an operation, performed for this or that disease.

Treatment of patients with external fistula is based on the following principles:

— local therapy;

— general therapy;

— operative therapy.

Local therapy — the treatment of a wound, protecting the surrounding tissue from the action of the fistula discharge. For this purpose physical means — ointments, pastes, powder (Lassar’s paste, glues BF-2, BF-6, polymerized film, silicone pastes), which are applied near the external apertures of the fistula to prevent contact with the skin and to promote discharge adsorption are used. Chemical means, prevention of skin irritation by neutralizing the enzymes secreted from the fistula, are used. With this purpose inhibitors of proteolytic enzymes (contrical, Gordoxum, Trasylolum, zymophren, etc.) are used. Mechanical ways of protecting the skin are directed on significant reduction or termination of fistula discharge with the help of special adaptations, such as pelotives, obturators or vacuums-devices. The sanitation of purulent fistulae is conducted with the help of constant washing with antiseptic solutions. Granulating tubular fistula can be closed independently after eliminating the cause of its arising — removing the ligatures, bone sequestration, and terminating the fistula discharge. The epitheliated fistulae never close independently and require surgical treatment — suturing the organ entrance, and sometimes resections of the given organ. Artificial fistulae are formed for improving the patient’s condition with the purpose of feeding him or discharge of the contents or secretion from the organ. These fistulae can be temporary or permanent. The temporary fistulae are closed surgically after the improvement of the patient’s condition. The inner artificial fistulae are interorgan anastomosis and are applied for a long time or for the whole life.