Gangrene: signs of the initial stage of gangrene of the lower extremities, gas gangrene, necrosis

Trophic foot ulcer develops against the background of various diseases: diabetes mellitus, essential thrombocytopenia, obliterating diseases of the lower extremities, varicose veins. In ICD 10, trophic foot ulcer is coded L97 (ulcer of the lower extremity, not classified elsewhere). Phlebologists at the Yusupov Hospital use a multidisciplinary approach to the treatment of trophic ulcers of the lower extremities.

Endocrinologists, vascular surgeons, and rheumatologists take part in the treatment process. Trophic foot ulcers that develop against the background of diabetic angiopathy heal after correction of blood glucose levels. Reversal of arterial ulcers occurs after restoration of blood flow through the arteries of the lower limb. A good effect in the treatment of venous trophic ulcers is observed after minimally invasive surgical interventions, which are masterfully performed by phlebologists at the Yusupov Hospital.

General information

What is gangrene? Gangrene is necrosis of body tissues/organs that develops due to lack of blood flow or the presence of a bacterial infection. Tissue necrosis - what is it? Necrosis is the death of tissue (organ), accompanied by irreversible changes and complete cessation of vital processes. In this case, it is necessary to distinguish between apoptosis and apoptosis . Like necrosis, apoptosis is a type of cell death in the body, but its main biological role is to establish a normal balance in tissues between the processes of cell death and their proliferation (Wikipedia). The main differences between apoptosis and necrosis are:

The process of apoptosis is determined genetically, necrosis is a pathological process.
Distribution of the process: the process of apoptosis extends exclusively to individual cells/groups of cells, while soft tissue necrosis can involve both individual tissue cells and the entire organ.
With apoptosis there is no inflammatory reaction (demarcation limiting inflammation), with necrosis it is present.
Morphological differences: during apoptosis - the formation of apoptotic bodies and their subsequent phagocytosis ; in case of necrosis, autolysis is caused by the action of hydrolytic enzymes.

The pathological anatomy of necrosis includes macro/microscopic signs.

Macroscopic signs are:

The presence of anesthetized dense dry tissue (during the process of mummification) or flabby/melted tissue (processes of myomalacia/encephalomalacia).
Change in tissue color to pale/white-yellow with a focus of necrosis in the myocardium, kidneys, spleen; dark red, soaked in blood (focus of necrosis in the lungs); stained with secretions (intestinal necrosis).
The presence of a bad odor (with putrefactive decay).

Microscopic signs of necrosis are characterized by specific changes in the cell/stroma:

In the cell nucleus there is karyepiknosis , wrinkling , disintegration and karyolysis .
In the cytoplasm of the cell, denaturation/coagulation of proteins, disintegration of the cytoplasm into clumps ( plasmorrhexis ) and hydrolytic melting of the cytoplasm ( plasmolysis ).
In the stroma - depolymerization of glycosaminoglycans, swelling, impregnation with plasma proteins, followed by melting.
Collagen fibers - swelling/impregnation with fibrin followed by disintegration; elastic fibers - swelling, disintegration, melting.
Formation of tissue detritus during the breakdown of cells/intercellular substance and demarcation inflammation around it.

Most often, gangrene affects the lower extremities, including fingers, feet or the entire limb, but can also develop in the muscles, internal/external organs - pulmonary gangrene , penile gangrene (Fournier’s gangrene), etc.

The following clinical and morphological forms of gangrene are distinguished:

Dry gangrene . It occurs predominantly against the background of slowly progressing ischemia in tissues with a relatively small fluid content (tissues of the upper/lower extremities). Dry necrosis, starting from the distal segments of the limb, progresses? gradually rising to the location of the blocked vessel, and in cases of well-developed collateral blood flow, necrosis may not rise to the site of blockage of the vessel. As a rule, a demarcation shaft is formed at the border of viable/dead tissue. When exposed to air, dead tissue dries out, thickens and shrinks, turning dark brown/black in color and becoming similar to mummy tissue. The phenomena of intoxication are insignificant, since decomposition products practically do not enter the bloodstream. In the initial stages, if pathogenic microflora attaches, there is a risk of transition to a wet form.
Wet gangrene. It develops more often against the background of rapid circulatory disturbances (for example, blockage of arterial trunks by emboli , vasoconstriction caused by thrombosis , spasm/anatomical changes in the vascular wall, impaired venous outflow, etc.) mainly in tissues containing a lot of moisture (lungs, intestines, gall bladder). The development of the disease is facilitated by the presence of concomitant pathologies - diabetes mellitus (diabetic gangrene), heart failure , kidney disease. Necrotic tissue does not have time to dry and putrefactive/purulent microflora quickly joins, for which dead tissue is a suitable nutrient medium, which contributes to its rapid development and spread of the process. The tissues swell/swell and emit the smell of rotting flesh, and the waste products of microorganisms and tissue breakdown enter the general bloodstream, causing severe intoxication.
Gas gangrene. Caused by pathogenic anaerobes of the genus Clostridium of various strains, mainly by the serovar Clostridium perfringens. They belong to spore-forming rods that are widespread in the external environment. The spores are highly resistant to external factors, but the clostridia themselves cannot exist for a long time in an oxygen environment.

The causative agent of gas gangrene releases exotoxins , causing necrotic changes in fatty tissue, muscles and connective tissue; hemolysis / thrombosis . Clostridial anaerobic infection is characterized by gas formation in the area of the pathological focus and rapid tissue swelling/necrosis. Gas containing carbon dioxide and hydrogen is the most important waste product of anaerobes. Tissue swelling contributes to an increase in pressure inside the fascial sheaths, which quickly causes muscle ischemia and contributes to their subsequent necrosis.

Infected edematous fluid and gas quickly spread through the perivascular/intermuscular tissue and, permeating the skin, exfoliate the epidermis, forming blisters filled with serous/hemorrhagic contents. The peculiarities and specificity of the course of wound infection can contribute to the predominant damage to subcutaneous fatty tissue or muscle tissue. Decomposition products, together with hemolyzed blood, imbibe the subcutaneous tissue, manifesting itself in the appearance of brown spots on the skin. Characteristic is the entry of tissue breakdown products/toxins into the systemic bloodstream, which is manifested by severe general intoxication/development of multiple organ failure. Sometimes the microbiology of wound surfaces is supplemented by a non-clostridial anaerobic infection, the so-called non-spore-forming “putrefactive infection”, the causative agents of which can be gram-negative bacilli, gram-positive/gram-negative cocci. Mixed anaerobic/aerobic infection is manifested by a sharp acceleration of the spread of the anaerobic-putrefactive process beyond the boundaries of the primary focus.

Types of gangrene of the feet

Two main types of pathology are considered:

Dry. If the layers of organs are left without oxygen for a long time, hypoxia will occur and the process of cell destruction will begin. The function of a body area is completely impaired, sensitivity is lost. There may be no pain - it all depends on the severity of the disease. The border zone is clearly defined, dead and living areas are separated.
Wet. It develops both independently and as a complication of dry gangrene. Elements of the skin become necrotic, the demarcation zone is unclear and blurred. Inflammation during gangrene leads to intoxication of the body. The symptoms are pronounced and dangerous.

The most severe form is gas gangrene. It develops due to the entry of anaerobic microbes into the wound. The infection spreads reactively throughout the body and without surgical intervention leads to amputation of a limb or death.

Pathogenesis

The pathogenesis of gangrene is determined by its specific type. Let us consider only the pathogenesis of dry gangrene of the extremities, which can be represented in several stages:

Stage of functional changes. It is characterized by a critical decrease in blood flow, which causes insufficient supply of oxygen/nutrients, leading to disruption of cellular energy processes and ischemia of a specific tissue area.
Stage of organic change. It is characterized by paralysis of the venous vessels, which develops compensatory to reduce the speed of blood flow in the tissues. As a consequence, excess blood accumulation develops in the venous system ( venous hyperemia ). Gradually, cell structures (nucleus, mitochondria, cell walls), stroma begin to collapse, and collagen/elastic fibers melt.
Necrotic stage. A section of tissue dies to the site of blockage of the vessel/area with bypass arteries. A zone of tissue demarcation/scarring is formed.

Diabetic gangrene

Diabetes mellitus is a common pathology associated with metabolic disorders. The disease can be of the first type, when insulin production is affected, and of the second, in which the problem lies in the membranes and channels of hepatocytes.

The main complication of diabetes is a change in the normal concentration of glycated hemoglobin, which leads to the destruction of the walls of blood vessels. Glucose becomes a trigger for the synthesis of increased amounts of glycosides and lipids. Plaques form, the lumen narrows, the supply of nutrients decreases, and hypoxia develops. Round small ulcers form on the skin, which threaten the development of necrosis.

Diabetic gangrene is characterized by:

Slow regeneration of damaged tissues.
Possibility of damage to blood vessels and nerves.
Involvement of bones in the process.

Gangrene progresses quickly and therefore requires urgent attention to a specialist. People with diabetes should closely monitor their health. At the initial stage, gangrene can be treated, and some tissues can recover. In case of late initiation of therapy, the consequences are very dire: from amputation of a limb or part thereof to death.

Classification

According to etiology there are:

Specific, resulting from certain diseases - diabetes mellitus (diabetic gangrene), tuberculosis , syphilis , leprosy , Fournier's gangrene (gangrene of the genital organs).
Nonspecific, developing after compression of tissues/vessels, extensive burns, wounds, due to thrombosis , embolism , surgical infection.

According to the degree of damage: superficial, deep, total.

According to the clinical course: dry, wet, gas gangrene.

Causes

The most common etiological factors for the development of gangrene are:

Circulatory disorders with the development of ischemia caused by injury, thrombosis, embolism and mechanical compression of blood vessels. Gradual disturbances in blood supply can develop with vascular spasm due to atherosclerosis , obliterating endarteritis (nicotine gangrene), cardiac dysfunction in the stage of decompensation, diabetes mellitus , etc.
Physical impacts that cause extensive injuries (mechanical, temperature effects) - burns , frostbite , electric shock, which destroy many cells/organs.
Chemical influences (alkalis/acids) causing disruption of the structure of proteins and their dissolution and saponification of fats.
Infectious effects. They develop when pathogenic aerobic/anaerobic microflora gets on the wound surface (with deep knife/gunshot wounds, crushing, crushing of tissues). The causative agents of gangrene can be Clostridia , Proteus , coccal flora , Escherichia coli , Enterobacteriaceae , etc.

Factors contributing to the development of gangrene include various disorders of the general condition of the body (intoxication, exhaustion, anemia, vitamin deficiency, acute/chronic infectious diseases, metabolic and blood composition disorders).

Symptoms

Of the various localizations of the gangrenous process, only gangrene of the lower extremities will be considered, as the most common. Code according to ICD-10, including the code for gangrene of the foot according to ICD-10: R02.

Dry gangrene of the lower extremities

How does gangrene of the leg begin? The first signs of gangrene of the lower extremities are characterized by increasing ischemic pain below the site of vessel occlusion. In cases of incomplete occlusion at the initial stage, the skin of the limb becomes atrophic, pale, cold to the touch, then marbled, sensitivity is reduced/completely lost, numbness periodically occurs, but pain persists even at the stage of pronounced necrotic changes. Prolonged pain syndrome in gangrene is due to the preservation of nerve cells in the foci of decay and compression of the nerve trunks caused by reactive edema of the proximal tissues from the lesion. The pulse in the peripheral arteries is practically undetectable. Characterized by impaired functioning of the limb. Most often, dry gangrene begins with the appearance of a small lesion on the toe of the extremity, which gradually spreads to the adjacent toes and the dorsum/plantar surface of the foot, involving more tissues of the extremity.

However, often the pathological process is limited, since dry gangrene is not prone to progression. And then we are talking about limited necrosis (gangrene of the foot or gangrene of the toe). At the same time, the symptoms of gangrene of the big toe, which often develops against the background of obliterating endarteritis / Raynaud's disease , begin with numbness of the toe and the appearance of a small initial lesion on it, which gradually spreads to the entire toe. The tissues involved in the process gradually shrink, decrease in volume, dry out, mummify and become denser, acquiring a dark brown or black color with a bluish tint. Demarcation (granulation) is constantly formed at the border of dead/healthy tissues. Since the conditions for the reproduction of pathogenic microflora in mummified tissues are unfavorable, the flow of toxic substances into the general bloodstream is insignificant, therefore intoxication is not pronounced and the general condition practically does not suffer. Below are photos of the initial stage of gangrene of the lower extremities.

Wet gangrene of the lower extremities

Wet gangrene begins with similar symptoms (cold limbs, pale skin, which then acquires a marble color). However, with wet gangrene, unlike dry gangrene, they do not thicken, the tissues become loose, swollen, quickly liquefy and disintegrate. The process involves skin, muscles, tendons, subcutaneous fat, fascia, and bones. Pathological occurs with a predominance of putrefactive fusion (infectious component). Skin hyperemia and edema quickly spread: the skin becomes shiny, can be tense, dark red spots quickly appear on it and blisters of exfoliated epidermis with ichorous contents form. The demarcation line is not formed independently. What gangrene looks like on the leg is shown in the photo below.

When examining the limb, the bluish venous network is clearly visible. There is no pulse in the peripheral arteries. Wet gangrene of the leg tends to generalize the process and, without treatment, quickly spreads, capturing adjacent areas of tissue.

Subsequently, the skin of the affected areas acquires a purplish-bluish color, turns black and disintegrates, forming a grayish-green foul-smelling mass. Due to the rapid entry into the general bloodstream of tissue breakdown products, signs of gangrene of the leg are complemented by an increase in intoxication and a sharp progression of deterioration in the general condition of the body. Severe pain, increased temperature, lethargy, decreased blood pressure , increased heart rate, lethargy, and dry mouth are noted. How long do patients live? In the absence of specialized care, sepsis and death occurs within 7-9 days. In old age, death may occur much earlier. Gangrene is especially severe in patients with diabetes , which is caused by metabolic disorders, a sharp deterioration in microcirculation and a decrease in the body's resistance.

Gas gangrene

The duration of incubation is determined by the type of pathogen and the form of the disease and can vary from 6 hours (fulminant forms) to 4 days. The disease manifests itself with the appearance of intense arching pain in the wound area. There is no pulse in the peripheral arteries. A specific sign is the patient’s complaint of a feeling of tightness from the applied bandage, which is due to the rapid increase/spread of swelling of the affected tissues. The swelling grows extremely quickly, and bloody fluid, reminiscent of meat slop, is released from the wound profusely. Subcutaneous fatty tissue has a gelatinous-jelly-like appearance with a greenish tint. The muscles bulge and become pale. The skin is shiny, sharply tense, and cold to the touch. Necrosis progresses rapidly (photo below).

The patient's condition quickly deteriorates: there is loss of appetite, general weakness, thirst, sleep disturbance, temperature up to 38-40°C, nausea, muscle aches, less often patients show anxiety or are very depressed. Visually pallor of the skin, less often with an earthy/jaundiced tint, sharpened facial features; characterized by increased body temperature, decreased blood pressure, rapid breathing , and tachycardia . Oliguria gradually develops , and later anuria .

Gangrene of other parts of the lower extremities

This phenomenon is accompanied by widespread necrosis. Diverse localization and etiology (atherosclerosis, diabetes, infection) makes diagnosis difficult. Pain syndrome appears in the later stages, which is why people most often turn to doctors at those stages of the progression of the disease when it is no longer possible to repair the damage.

It is worth understanding that the gangrenous process causes charring and cell death; it will not stop on its own. All layers of the skin are damaged. Blood circulation is severely disrupted.

Bedsores are common on the lower extremities and back. These are areas of necrosis caused by acute hypoxia due to strong compression of tissues by the weight of one’s own body. To avoid trouble, caregivers of a bedridden patient must understand the importance of prevention, frequent turning over of the patient and changing positions.

Prevention

Prevention of gangrene comes down to measures such as:

Timely detection and adequate treatment of various diseases/pathological conditions that are accompanied by impaired blood supply ( diabetes mellitus , thrombophlebitis of the lower extremities , cardiac disorders in the stage of decompensation, etc.).
Injury prevention.
Timely radical primary surgical treatment of wound surfaces, observing the rules of asepsis during invasive manipulations.
To give up smoking.

Prevention of gas gangrene involves the administration of anti-gangrenous polyvalent/monovalent serums after wound treatment.

Gangrene of the toes

Often the disease begins with the little finger. The fingers gradually turn black: the lesions initially look like small spots.

The reactive progression of the anomaly is facilitated by the possibility of gangrene spreading along the nerves. This fact makes the pathology especially dangerous: the process cannot always be tracked and stopped in a timely manner even by highly qualified specialists. The lower extremities are well innervated, so the disease has many ways of spreading (compared with the number of nerve fibers in the affected area). In severe cases, gangrene of the finger can lead to amputation of the entire limb.

List of sources

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