Trophic ulcers

Trophic ulcer (ulcus) is a defect of the skin or mucous membrane, which is characterized by a chronic course without a tendency to spontaneous healing or periodic recurrence. Among the numerous purulent-necrotic diseases of the lower extremities, trophic ulcers occupy a special position due to their widespread occurrence and complexity of treatment. "Ulcers of the leg represent a true cross for surgeons due to their enormous persistence and difficulty of treatment," wrote S. I. Spasokukotsky at the beginning of the last century. However, this problem has not lost its relevance to this day.

In European and North American countries, at least 0.8-1.5% of the population suffers from venous ulcers of the lower extremities alone, and in the age group over 65 years, the incidence reaches 3.6%. The costs associated with the treatment of ulcers make up 1-2% of the health care budget of these countries. Persistent, long-term course of the disease, development of complications often leads to loss of ability to work. Disability is established in 10-67% of patients with ulcers of the lower extremities.

Ulcer formation should be discussed if the skin defect does not heal within six weeks or more. The pathogenesis of the formation of most ulcers has not been sufficiently studied, although much is already known. One of its main links is considered to be a violation of the blood supply to tissues as a result of the following reasons: decreased blood flow and oxygen delivery, blood shunting, venous and lymphatic outflow disorders, metabolic and exchange disorders, infectious, autoimmune processes, etc.

Trophic ulcers are located on the lower extremities in more than 95% of cases. Their appearance on the upper extremities, trunk and head occurs much less frequently and is usually not associated with any vascular diseases. A skin trophic ulcer is not considered an independent pathological condition, but a complication of various (more than 300) diseases and syndromes. The cause of ulcer formation can be various congenital or acquired vascular diseases, consequences of injuries, infections, general diseases and other factors, which are often very difficult to systematize due to the huge number of diseases and conditions leading to the development of an ulcer defect. Below is a classification of the main diseases in skin ulcer syndrome.

What causes trophic ulcers?

The most common cause is varicose insufficiency, followed by arterial insufficiency, neuropathy, diabetes mellitus. Risk factors include a sedentary lifestyle, injuries, and exhaustion.

Varicose trophic ulcers occur after deep vein thrombosis, failure of superficial or perforating vein valves. In venous hypertension, capillaries become tortuous, their permeability to large molecules increases, and fibrin is deposited in the perivascular space. This disrupts the diffusion of oxygen and nutrients, which contributes to ischemia and necrosis. Minor injuries (bruises and scratches) and contact dermatitis provoke the formation of ulcers.

Neurotrophic ulcers (diabetic foot) are caused by ischemia combined with sensory neuropathy. Due to abnormal pressure distribution on the foot, calluses form on bony prominences, which subsequently ulcerate and quickly become infected.

In addition, the hereditary factor is of great importance. As a rule, half of patients with trophic ulcers of the legs also have close relatives who suffer from it. Possibly, the weakness of the connective tissue and the venous valve flaps formed by it is inherited.

Mixed trophic ulcers

Mixed trophic ulcers are the result of the influence of several etiologic factors on the ulcer formation process. They constitute at least 15% of all ulcerative defects of the lower extremities. The most common variants are those that combine pathology of arteries and veins, arteries and diabetic neuropathy, pathology of veins and severe circulatory failure.

When diagnosing mixed ulcers, it is first necessary to determine the role of each of the etiologic factors and identify the priority pathology. Treatment should be aimed at correcting all pathogenetic links that form a skin ulcer. In the presence of arterial pathology, identifying the degree of arterial insufficiency is considered a decisive factor determining surgical tactics, due to the real or potential danger of limb loss.

In congestive heart failure, trophic ulcers usually develop on both extremities, are multiple, extensive, and exude abundantly. This type of skin ulcer usually affects elderly and senile patients. The real prospects for healing such ulcers can only be assessed after compensation for circulatory failure and elimination of edema. Due to the presence of extensive tissue lesions in the extremities, developing against the background of severe circulatory failure in combination with chronic venous insufficiency or arterial insufficiency, the prospects for healing such ulcers are extremely small. In most cases, success should be considered the elimination of the inflammatory process, a decrease in exudation, the transition of the wound process to stage II, and the elimination of pain.

Of particular relevance are mixed trophic ulcers of arterial-venous etiology, which are detected most frequently. They present certain difficulties for diagnosis and treatment.

Hypertensive-ischemic trophic ulcer

Hypertensive-ischemic trophic ulcer (Martorell) accounts for no more than 2% of all ulcerative-necrotic lesions of the lower extremities. It occurs in patients with severe forms of arterial hypertension as a result of hyalinosis of small arterial trunks in the skin of the lower extremities. Ulcers of this etiology are usually detected in women aged 50-60 years.

Long-term hypertension leads to damage of arterioles, as a result of which blood flow in this area of skin weakens. In case of blood microcirculation disorders, increased permeability of the vascular membrane, formation of local microthromboses, ending with formation of soft tissue necrosis, are noted. Trophic ulcer is usually located on the outer or back surface of the shin. They often occur on symmetrical areas of the shins. Ulcers are characterized by sharp pain both at rest and on palpation. Ulceration begins with the formation of purple papules or plaques, which then turn into hemorrhagic bullae. Primary skin elements dry out over time and transform into a dry necrotic scab with involvement of the skin and upper layers of subcutaneous tissue in the pathological process. Perifocal inflammation is usually not expressed.

In Martorell's trophic ulcer, hemodynamically significant disorders of the main arterial blood flow, pathological venovenous refluxes determined clinically, by ultrasound Dopplerography and duplex angioscanning are not observed. To establish the correct diagnosis, it is necessary to exclude all other causes that can lead to the development of an ulcerative defect of the leg (diabetes mellitus, obliterating thromboangiitis and atherosclerosis, chronic venous insufficiency, etc.), with the exception of hypertension.

Martorell's trophic ulcer is characterized by the duration of the first phase of the wound process, resistance to various methods and means of local and general therapy. Treatment is of little promise without stable stabilization of blood pressure. In local therapy, in the presence of dry necrotic scab, preference is given to hydrogel dressings. In case of extensive trophic ulcers in the second stage of the wound process, the possibility of autodermoplasty is considered.

Pyogenic trophic ulcers

Pyogenic trophic ulcers occur against the background of non-specific purulent diseases of soft tissues (pyoderma, infected wounds, etc.) in patients from socially disadvantaged groups of the population. This type of ulcers can also include long-term non-healing skin defects that have arisen after complicated erysipelas, carbuncle, abscess and phlegmon. In their classic form, pyogenic trophic ulcers are multiple superficial purulent foci that have a round shape and are covered with a thick purulent coating with a pronounced perifocal inflammatory reaction. An important diagnostic criterion is considered to be the syndrome of systemic inflammatory reaction in the absence of signs of damage to the vascular systems of the limb and other causes of ulcer formation. The development of trophic ulcers is usually caused by gram-positive cocci Staphylococcus aureus, Streptococcus spp., much less often - Pseudomonas aeruginosa and other gram-negative rods.

Pyogenic trophic ulcers usually have a long, persistent course. The main methods of treatment are surgical treatment of the purulent focus, antibacterial therapy (protected semi-synthetic penicillins (amoxiclav 625 mg 2 times a day), cephalosporins of the II-III generation, etc.), general strengthening and local therapy. In the case of extensive skin defects, skin plastic surgery is performed.

Post-traumatic trophic ulcers

Posttraumatic trophic ulcers are a rather heterogeneous group of chronic skin defects that occur after surgical interventions, various mechanical, thermal, radiation and other skin injuries. In recent years, cases of post-injection ulcers of the extremities in patients with drug addiction have become more frequent. It is necessary to distinguish trophic ulcers that occur after a sufficiently strong impact of a traumatic agent that caused severe local microcirculation disorders from ulcerative defects that developed after an injury against the background of venous, arterial, neurological and other pathologies.

The main method of treating post-traumatic ulcers is excision of scar-trophic tissues with skin grafting of the defect. To close most defects, local tissue grafting and combined methods are used. If it is necessary to close ulcers on the supporting surfaces of the limb, in the area of joints, and in the case of radiation ulcers, full-layer vascularized flaps are used, for which dosed tissue stretching, rotational skin-fascial flaps, Italian skin grafting, Filatov stem, and free flap transplantation on microvascular anastomoses are used.

Trophic ulcers against the background of malignant neoplasms

Trophic ulcers against the background of malignant neoplasms are found in approximately 1-1.5% of cases. They arise as a result of the disintegration and ulceration of skin tumors (melanoma, basal cell carcinoma, etc.), malignant tumors of soft tissues and bones (adenocarcinoma of the mammary gland, fibrosarcoma, rhabdomyosarcoma, osteosarcoma, etc.), metastases of various tumors to the skin and subcutaneous lymph nodes. In a number of patients with tumors of internal organs and leukemia, trophic ulcers develop as a result of ulcerative-necrotic vasculitis, which is considered one of the most striking manifestations of paraneoplastic syndrome.

Such trophic ulcers have uneven, undermined edges, the bottom is deep, crater-shaped, infiltrated, filled with necrosis, abundant foul-smelling discharge. To verify the diagnosis, a histological examination of biopsies taken from the edges is carried out. Treatment of such patients is mainly carried out by oncologists and dermatologists.

Treatment methods for this large and diverse group depend on the stage of the malignant disease. In the absence of distant metastasis, wide excision of the affected tissues with skin grafting of the wound defect or amputation (exarticulation) of the limb, regional lymphadenectomy are performed. In the event of complications in the form of bleeding, tumor disintegration accompanied by intoxication, palliative interventions are possible in the form of partial or complete tumor removal, limb amputation, simple mastectomy. These interventions allow patients to prolong their lives and improve their quality of life.

The prognosis for recovery depends on the stage of the oncological process and is associated with the possibility of radical intervention. Since skin ulcers in malignant diseases are in most cases a sign of a late stage of the disease, the prognosis is generally unfavorable not only for the healing of the trophic ulcer, but also in terms of the duration and quality of life.

Trophic ulcers against the background of systemic diseases of connective tissue

Trophic ulcers against the background of systemic connective tissue diseases usually have no specific signs. To identify the nature, diagnostics of the underlying disease is of great importance. Targeted examination of patients should be carried out in case of prolonged atypical ulcers without a tendency to regeneration, as well as in case of detection of syndromes indicating systemic autoimmune damage to organs and tissues (polyarthritis, polyserositis, damage to the kidneys, heart, lungs, eyes, etc.). Trophic ulcers occur against the background of a skin syndrome, which is present to varying degrees in patients with collagenoses. The skin defect occurs as a result of necrotic vasculitis. Trophic ulcers most often affect the lower extremities (shin, foot), but atypical localization is also possible (thighs, buttocks, trunk, upper extremities, head, oral mucosa).

Trophic ulcers against the background of other diseases

Trophic ulcers that develop against the background of gangrenous pyoderma have some clinical features. They most often occur in patients with Crohn's disease and nonspecific ulcerative colitis. In approximately 10% of such patients, gangrenous pyoderma is one of the most severe extraintestinal manifestations. Such ulcers are characterized by the presence of multiple, sharply painful, purulent-necrotic skin defects that gradually increase in size. The edges of the trophic ulcer have bluish, corroded edges and a ring of hyperemia. Trophic ulcers are localized mainly on the feet and shins.

In 30% of patients, ulcerative defects may form on the buttocks, trunk, and upper limbs.

Trophic ulcers are characterized by persistent lupus erythematosus with a prolonged phase I of the wound process. Regenerative capabilities are sharply reduced, which is associated with both the course of the underlying disease and the standard therapy (corticosteroid hormones, cytostatics, etc.). When the patient's condition stabilizes with the achievement of stable remission, autodermoplasty not only significantly accelerates the healing of extensive ulcerative defects, but also makes this healing the only possible one. In patients with a progressive nature of the underlying disease, the prospect of their closure is extremely low.

Trophic ulcers, against the background of other, rarer diseases, are detected in no more than 1% of cases, but they are the ones that cause the greatest difficulties in diagnosis.

Their diagnosis requires a thorough study of the anamnesis, recognition of the underlying disease. Special examination should be carried out in case of prolonged atypical or progressive ulcers without a tendency to regeneration. In doubtful cases, biochemical, serological, immunological, histological and other research methods are indicated, allowing to identify the nature of the underlying disease.

Symptoms of trophic ulcers

The most common is a varicose trophic ulcer. Against the background of tissue compaction and edema, deep and superficial ulcers are formed, round, oval or polycyclic in shape, ranging in size from 2-3 to 5-10 cm or more. The edges of the ulcers are uneven and undermined. They are often localized in the lower third or on the anterolateral surface of the leg. Trophic ulcers are characterized by a torpid course, and secondary infection (erysipelas or phlegmon) is quite common. The bottom is covered with serous-purulent discharge, flaccid granulations, accompanied by pain.

Ischemic trophic ulcers have steep, clearly defined edges, their bottom is usually covered with a scab, under which tendons are visible. The discharge is scanty. Other signs of ischemia are the absence of hair on the foot and shin, shiny atrophic skin: there is no hyperpigmentation, no sclerosis of the skin and subcutaneous tissue. The bottom is dry - gray or black. On palpation, pain and the absence or weakening of the pulse in the peripheral arteries are noted. Trophic ulcers are often located above the ankles and bony prominences, on the toes.

In neurotrophic ulcers, the skin of the foot is dry, warm, there is no sensitivity, and the pulse on the arteries is preserved. Trophic ulcers are deep, often with callused edges, there is edema caused by damage to the sympathetic nerves and constant vasodilation. The bottom is dry - gray or black. When palpating, first on the big toes, and then on the feet, sensitivity is lost. Later, the Achilles reflex and proprioceptive sensitivity disappear. Trophic ulcers are localized in frequently injured, deformed areas of the feet, soles, heels and big toe.

Classification of ulcerative-erosive skin lesions by etiology

I. Trophic ulcer caused by chronic venous insufficiency against the background of:

• post-thrombophlebitic disease;
• varicose veins;
• congenital venous angiodysplasia, Klippel-Trenaunay syndrome.

II. Trophic ulcer caused by diseases of the arteries of the lower extremities (ischemic trophic ulcer):

• against the background of macroangiopathies:
• obliterating atherosclerosis of the vessels of the lower extremities;
• thromboangiitis obliterans (Buerger-Winiwarter disease),
• postembolic occlusion of arteries of the lower extremities.
• trophic ulcer against the background of microangiopathy:
• diabetic trophic ulcer;
• hypertensive-ischemic trophic ulcer (Martorell syndrome).

III. Trophic ulcer caused by arteriovenous fistulas:

• congenital (Parkes Weber syndrome);
• post-traumatic trophic ulcer.

IV. Trophic ulcer against the background of impaired lymphatic drainage:

• primary lymphedema (Milroy's disease, etc.);
• secondary lymphedema (after erysipelas, surgery, radiation therapy, etc.);
• lymphedema due to filariasis, etc.

V. Post-traumatic trophic ulcer:

• after chemical, thermal and electrical injuries;
• due to mechanical and gunshot damage to soft tissues;
• as a result of bites from humans, animals and insects;
• osteomyelitic;
• decubital;
• amputation stumps of the foot, lower leg, thigh;
• postoperative scars (cicatricial trophic ulcers);
• post-injection;
• radial.

VI. Neurotrophic ulcer:

• due to diseases and injuries of the brain and spinal cord;
• caused by damage to peripheral nerve trunks;
• against the background of infectious, congenital, toxic, diabetic and other polyneuropathies.

VII. Trophic ulcer arising against the background of general diseases:

• systemic diseases of connective tissue (collagenoses) and similar diseases and syndromes (rheumatoid polyarthritis, systemic lupus erythematosus, dermatomyositis, scleroderma, periarteritis nodosa, Raynaud's disease, Wegener's granulomatosis, Crohn's disease, antiphospholipid syndrome, cryoglobulinemia, gangrenous pyoderma, etc.);
• chronic diseases of the cardiovascular system (ischemic heart disease, heart defects, cardiomyopathy, etc.), occurring with severe circulatory failure;
• chronic liver and kidney diseases;
• severe chronic anemia and other blood diseases (sickle cell anemia, hereditary spherocytosis, thalassemia, etc.);
• endocrinopathies (“steroid” ulcers, etc.);
• metabolic diseases (gout, amyloidosis, etc.);
• avitaminosis and alimentary exhaustion.

VIII. Trophic ulcer caused by infectious, viral, mycotic and parasitic diseases of the skin:

• tuberculous (indurated erythema of Bazin, colliquative tuberculosis of the skin, scrofuloderma, etc.), syphilitic, leprosy, anthrax, Lyme disease (borreliosis), glanders, melioidosis, cutaneous leishmaniasis (Borovsky's disease), nocardiosis, epithelioid angiomatosis (cat scratch disease), etc.;
• erosive and ulcerative lesions of herpes simplex or varicella zoster,
• mycotic (fungal);
• pyogenic, developed in connection with non-specific infectious diseases of the skin and subcutaneous tissue (phlegmon, erysipelas, pyoderma, etc.).

IX. Trophic ulcer that occurs against the background of neoplasms:

• benign skin neoplasms (papillomas, nevi, fibromas, etc.);
• malignant neoplasms of the skin and soft tissues (Kaposi's sarcoma and other sarcomas, melanoma, basal cell carcinoma, etc.);
• blood diseases - ulcerative necrotic vasculitis (hemorrhagic vasculitis, Henoch-Schonlein hemorrhagic purpura, leukemia, mycosis fungoides, agranulocytosis, etc.);
• malignant neoplasms of internal organs;
• disintegration of malignant tumors (for example, breast cancer, etc.) and metastases to the skin and subcutaneous lymph nodes.

X. Trophic ulcer and ulcerative-erosive skin lesions that arise against the background of acute and chronic skin diseases - eczema, dermatitis, psoriasis, vesicular dermatoses, etc.

XI. Artificial trophic ulcer due to self-mutilation, pathomimia, introduction of foreign bodies, injections of narcotic and other substances, etc.

XII. Mixed trophic ulcer, combining several causes.

XIII. Chronic trophic ulcer of another, difficult to classify etiology.

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Complications of trophic ulcers

Long-term existence of an ulcer defect often leads to various complications, which are considered the main reason for emergency hospitalization of a significant portion of patients. The main complications include:

• dermatitis, eczema, cellulitis, pyoderma;
• erysipelas, phlegmon, anaerobic infection;
• tendinitis, periostitis, contact osteomyelitis;
• thrombophlebitis; lymphangitis, regional lymphadenitis, secondary lymphedema;
• arthritis, arthrosis;
• tetanus;
• bleeding;
• malignancy;
• Infestation with insect larvae (wound myiasis).

In case of inadequate local therapy of ulcers using ointment-based preparations, as well as insufficient hygiene, periulcer complications in the form of dermatitis, eczema, cellulitis and pyoderma are possible. In this case, in the acute phase of inflammation, diffuse hyperemia, infiltration, oozing with the development of erosions and pustules appear on the skin in the circumference. At this stage, previously used dressings should be abandoned and wet-drying dressings with iodophor antiseptics (iodopyrone, povidone-iodine, etc.) or absorbent multilayer dressings should be used. Dressings should be changed 1-2 times a day. Glucocorticoid ointments, creams, pastes or mixtures containing salicylates (zinc oxide, salicylic-zinc paste) [lotion or ointments (diprosalik, belosalik, etc.)] are applied to inflamed skin (but not to the ulcer!) Most often, skin-inflammatory complications occur in patients with venous trophic ulcers in the first phase of the wound process.

Various forms of erysipelas and its complications, lymphangitis and inguinal lymphadenitis are most typical for patients with venous trophic ulcers and often serve as an indication for hospitalization of patients. Erysipelas is characterized by an acute onset with a predominance of intoxication symptoms at the first stages, accompanied by chills, high fever, and severe weakness. A little later, characteristic local changes occur in the form of diffuse hyperemia of the skin with more or less clear boundaries of an uneven shape. The skin is infiltrated, edematous, hot to the touch, painful, and rises in the form of a ridge above the unaffected areas of the skin. Confluent superficial blisters with serous exudate may occur against the background of erythema erysipelas. In more severe cases, hemorrhages ranging in size from small petechiae to extensive hemorrhages with the formation of confluent blisters filled with serous-hemorrhagic exudate are observed; truncular lymphangitis of the lower thigh and inguinal lymphadenitis develop. The main methods of treating these complications are considered to be antibacterial therapy (semi-synthetic penicillins, cephalosporins, etc.), adequate local therapy and physiotherapy (UV irradiation). Relapses of erysipelas lead to the development of lymphedema of the limb. To prevent relapses of erysipelas, it is necessary to heal the ulcerative defect (entry gate of infection) and monthly administration of prolonged synthetic penicillins (retarpen or extencellin 2.4 million IU).

In the presence of deep, poorly drained ulcerative defects, such a severe complication as phlegmon often develops. The disease is accompanied by the development or significant increase in pain syndrome, the appearance of severe edema and diffuse hyperemia, sharp pain during palpation, and sometimes fluctuation of soft tissues. Symptoms of severe intoxication with febrile fever, high leukocytosis and neutrophilia are noted. Phlegmon is most often diagnosed in patients with diabetic and osteomyelitic lesions. With the development of phlegmon, urgent surgical treatment of the purulent focus is indicated, as well as the appointment of antibacterial and infusion-detoxification therapy.

Anaerobic clostridial and non-clostridial infection is considered the most severe complication. Most often, it occurs against the background of limb ischemia, with inadequate care of the ulcer defect, local application of fat-based ointments (Vishnevsky ointment, etc.). The infection develops quickly, occupies significant areas of the limb with the development of necrotic dermatocellulitis, fasciitis and myositis, it is accompanied by a pronounced systemic inflammatory reaction and severe sepsis. Delayed diagnosis and late hospitalization lead to frequent loss of limb and high mortality, reaching 50%.

In conditions of a long-standing ulcerative defect, the destructive process can spread to the deep layers of soft tissues with the development of tendinitis, periostitis, contact osteomyelitis, purulent arthritis, which significantly complicate the possibility of independent healing of a chronic wound.

Bleeding occurs more often in patients with chronic venous insufficiency as a result of erosion of the subcutaneous vein located at the edges or at the bottom of a trophic ulcer. Recurrent bleeding often occurs in patients with malignant trophic ulcers or against the background of malignant neoplasms of the skin and soft tissues. Blood loss can be significant, up to the development of hemorrhagic shock. In case of erosion of a sufficiently large vessel and active bleeding, the bleeding area should be sutured or the vessel should be ligated along its length. However, in most cases, adequate hemostasis requires applying a pressure bandage with a hemostatic sponge, elastic bandaging, and an elevated position of the limb. Hemostasis is possible with the help of phlebosclerosing therapy.

Malignancy is observed in 1.6-3.5% of cases.

Predisposing factors to malignancy include long-term existence of a trophic ulcer (usually more than 15-20 years), frequent relapses, inadequate therapy with ointments containing irritants (Vishnevsky ointment, ichthyol ointment, etc.), frequent ultraviolet and laser irradiation of the ulcer surface. Malignancy is suspected in the absence of positive dynamics in healing, with rapid progression, the appearance of excess tissue areas rising above the wound, the occurrence of foci of putrefactive tissue destruction with the appearance of necrosis, foul-smelling discharge, and increased bleeding. The diagnosis is verified by biopsy of various suspicious areas of the edges and bottom.

Many specialists do not consider wound myiasis as a complication, moreover, insect larvae are specifically used to perform necrectomy of heavily contaminated ulcers. This method is called biosurgery. However, it is hardly worth considering this method as a serious alternative to more effective, cheap and aesthetic modern methods of ulcer cleansing.

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How to recognize trophic ulcers?

Trophic ulcer is one of the most severe complications of the underlying disease, against which they develop. The fundamental point of diagnosis is the determination of the etiology, which makes it possible to carry out adequate etiotropic or pathogenetic therapy.

In most cases, characteristic clinical symptoms allow to establish the true cause of the formation already at the first examination of the patient. Diagnostics is based on anamnestic information, results of examination of the patient and the area of skin changes, data of instrumental and laboratory research methods. When making a diagnosis, clinical signs and features of the local lesion characteristic of a particular pathology are taken into account. Thus, detection of an ulcerative defect in the area of the medial malleolus, accompanied by hyperpigmentation and induration of the surrounding skin, varicose syndrome, with a high degree of probability indicates the development of a trophic ulcer against the background of chronic venous insufficiency. The occurrence of an ulcer on the plantar surface of the foot in a patient with impaired skin sensitivity allows to reasonably suspect the neurotrophic genesis of the ulcer. In some cases, especially with an atypical course of ulcerative lesion, as well as to clarify the nature of the underlying disease, instrumental and laboratory diagnostic methods are necessary. In case of vascular (venous and arterial) lesions, the main diagnostic methods are considered to be ultrasound Dopplerography and duplex scanning, in case of osteomyelitic lesions - X-ray of bones, and in case of lesions caused by malignant neoplasms - cytological and histological methods.

No less important is the assessment of the ulcer defect itself with a detailed description of its localization, size, depth, stage of the wound process and other parameters that may be specific to the underlying disease, reflect the dynamics and effectiveness of treatment. For this purpose, a visual assessment of the ulcer and surrounding tissues with a description of all existing changes, planimetric methods, photography and digital photometry are used.

The size of the ulcer, the depth of the defect, its localization, the volume and severity of microcirculatory changes in the surrounding tissues, the development of infection are important factors in determining the severity of the disease and its prognosis. The depth and area of a skin ulcer may vary. Depending on the depth of tissue destruction associated with the ulcerative process, a distinction is made between:

• Grade I - superficial ulcer (erosion) within the dermis;
• II degree - an ulcer reaching the subcutaneous tissue;
• Grade III - an ulcer that penetrates to the fascia or extends to subfascial structures (muscles, tendons, ligaments, bones), penetrating into the cavity of the joint capsule, joint or internal organs.

Depending on the size, there are:

• small trophic ulcer, area up to 5 cm2;
• average - from 5 to 20 cm2;
• large trophic ulcer - from 20 to 50 cm2;
• extensive (giant) - over 50 cm2.

The prospects for healing an ulcer defect largely depend on the severity of blood flow disorders in the skin around the ulcer. In some situations, even when the main causes leading to ulcer formation are eliminated, irreversible microcirculation disorders develop in the surrounding tissues, which do not leave any opportunities for spontaneous healing of the skin defect. The main methods for diagnosing microcirculatory disorders are measuring transcutaneous oxygen tension, laser Doppler flowmetry, and thermometry.

All ulcer defects are infected. In case of pyogenic ulcers, the infectious factor is the leading one in the origin of the disease. In phase I of the wound process, dynamic assessment of the infectious factor supporting inflammation is extremely important for identifying bacterial or fungal pathogens and selecting targeted antibacterial therapy. For this purpose, smear microscopy is performed, which allows for the composition of the microflora and its quantity, sensitivity to antibiotics to be determined in a short time. If malignancy of the ulcer or its malignant nature is suspected, histological examination of biopsies taken from suspicious areas of the edges and bottom of the ulcer is performed. Other diagnostic methods are used according to indications or in case of detection of rare causes of ulcer formation that require the use of additional diagnostic methods.

The construction of a clinical diagnosis for trophic ulcer should reflect the features of the underlying disease, its complications according to the international classification of diseases. For example, post-thrombophlebitic disease of the lower extremities, recanalized form, chronic venous insufficiency class VI, extensive trophic ulcer, dermatitis of the left shin; or obliterating atherosclerosis of the vessels of the lower extremities, occlusion of the iliofemoral segment on the right, chronic arterial insufficiency grade IV, trophic ulcer of the dorsum of the foot; or diabetes mellitus type II, severe course, decompensation stage, diabetic nephropathy, retinopathy, diabetic foot syndrome, neuropathic form, plantar trophic ulcer, cellulitis of the left foot.

Differential diagnostics of trophic ulcers

When conducting differential diagnostics, it should be borne in mind that most lower limb ulcers (80-95%) are venous, arterial, diabetic or mixed. Other diseases should be suspected only after excluding the main causes or in case of ineffectiveness of standard therapy. One of the main differential diagnostic techniques is determining the pulsation in the arteries of the lower limbs, which must be carried out on all patients with ulcerative defects.

Trophic ulcers should be distinguished from nodular periarteritis, nodular vasculitis, malignant neoplasms (basal cell and squamous cell skin cancer, skin lymphomas), injuries, bedsores, gangrenous pyoderma, etc.

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Treatment of trophic ulcers

Treatment of trophic ulcers is carried out taking into account the principles of therapy of skin diseases. Treatment of varicose ulcers requires therapy of the underlying disease, phlebectomy or daily wearing of elastic stockings, to reduce venous pressure - elevated position of the legs. Zinc-gelatin bandage is applied weekly. It is necessary to treat the phenomena of dermatitis, eczema in accordance with the manifestations of the skin pathological process, remove necrotic tissue. In case of infection of foci, broad-spectrum antibiotics are prescribed. Skin transplantation is used.

For the treatment of ischemic ulcers, drugs are recommended that improve blood supply in the arteries, and arterial hypertension is treated. For radical cure, reconstructive operations on the arteries are used.

Trophic ulcers in a patient with idiopathic progressive skin atrophy.

In the treatment of trophic ulcers, special attention should be paid to the use of vitamins, antihistamines, and biogenic stimulants. The inclusion of phlogenzym (2 capsules 3 times a day) significantly increases the effectiveness of treatment.

In case of long-term non-healing trophic ulcers, it is recommended to prescribe corticosteroids orally in low doses (25-30 mg per day). Physiotherapeutic procedures (helium-neon laser, UV radiation, zinc ion galvanization, local mud baths, etc.) are widely used, and externally - agents that improve tissue trophism (solcoseryl, actovegin, etc.), which promote ulcer epithelialization.

Treatment of trophic ulcers is a difficult task, in some cases with poorly predictable results. In a large number of observations, they remain resistant to modern methods of complex surgical and conservative treatment. That is why the priority should be early detection of the underlying disease and adequate preventive therapy to prevent the disease from progressing to advanced stages, resulting in the formation of an ulcer defect.