Trophic ulcers

Trophic ulcer (ulcus) is a defect in the skin or mucosa, which is characterized by a chronic course with no tendency to spontaneous healing or recurrent recurrence. Among the numerous purulent-necrotic diseases of the lower extremities, trophic ulcers occupy a special position because of their wide spread and complexity of treatment. "Ulcers of the shin represent a true cross of surgeons because of their enormous persistence and difficulty in healing," the SI wrote. Spasokukotsky at the beginning of the last century. However, to this day this problem has not lost its relevance.

In Europe and North America, only venous ulcers of the lower extremities suffer at least 0.8-1.5% of the population, and in the age group over 65, the frequency reaches 3.6%. The costs associated with the treatment of ulcers are 1-2% of the health budget of these states. Persistant, prolonged course of the disease, the development of complications often leads to disability. Disability is established in 10-67% of patients with ulcers of the lower extremities.

On the formation of ulcers should be said in the event that the skin defect does not heal for six weeks or more. The pathogenesis of the formation of most ulcers has not been studied enough, although much has already been learned. One of its main links is the violation of blood supply to tissues due to the following reasons: decrease in blood flow and oxygen delivery, shunting of blood, violations of venous and lymphatic outflow, metabolic and metabolic disorders, infectious, autoimmune processes, etc.

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

What causes trophic ulcers?

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

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

Neurotrophic ulcers (diabetic foot) occur as a result of ischemia in combination with sensory neuropathy. Because of the abnormal pressure distribution on the foot, bone marrow is formed on the bony protuberances, which subsequently ulcerate and quickly become infected.

In addition, the hereditary factor is of great importance. As a rule, half of patients with trophic leg ulcers also suffer from close relatives. It is possible that the weakness of the connective tissue and the valves of venous valves formed by it are inherited.

Mixed trophic ulcers

Mixed trophic ulcers - the result of the influence of several etiological factors on the process of ulceration. They account for not less than 15% of all ulcerative defects of the lower extremities. The most common variants that combine the pathology of the arteries and veins, arteries and diabetic neuropathy, the pathology of veins and severe circulatory insufficiency.

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

With congestive heart failure, trophic ulcers usually develop on both extremities, they are numerous, extensive, abundantly exuding. This kind of skin ulcers usually affects elderly and senile patients. The real prospects for healing such ulcers can be assessed only after compensating for circulatory failure and eliminating edema. In view of the presence of a vast amount of lesions of limb tissues developing against a background of severe circulatory insufficiency combined with chronic venous insufficiency or arterial insufficiency, the prospects for healing such ulcers are extremely small. In most cases, the 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 the pain syndrome.

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

Hypertensive-ischemic trophic ulcer

Hypertensive-ischemic trophic ulcer (Martorel) is not 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 limbs. Ulceration of this etiology is usually detected in women aged 50-60 years.

Prolonged hypertension leads to the defeat of arterioles, as a result of which the blood flow in this area of the skin weakens. With violations of blood microcirculation, an increased permeability of the vascular membrane, the formation of local microthrombosis, resulting in the formation of necrosis of soft tissues. The trophic ulcer is usually located on the outer or posterior surface of the tibia. Often, it occurs in the symmetrical areas of the shins. Ulcers are characterized by a sharp soreness in both rest and palpation. Ulceration begins with the formation of violet papules or plaques, which then turn into hemorrhagic bullae. Primary skin elements eventually dry up and transform into a dry necrotic scab, involving the skin and upper layers of subcutaneous tissue in the pathological process. Perifocal inflammation is usually not expressed.

With the trophic ulcer Martorel hemodynamically significant disorders of the main arterial blood flow, pathological veno-venous reflux, determined clinically, with ultrasound Doppler and duplex angioscanning, do not. To establish the correct diagnosis, it is necessary to exclude all other causes that may lead to the development of a ulcerative shin defect (diabetes mellitus, thromboangiitis obliterans and atherosclerosis, chronic venous insufficiency, etc.), with the exception of hypertension.

The trophic ulcer of Martorel is characterized by the duration of the course of the I phase of the wound process, its resistance to various methods and means of local and general therapy. Treatment is not very promising without stable BP stabilization. In local therapy, in the presence of dry necrotic scab, hydrogel dressings are preferred. With extensive trophic ulcers, which are in the II stage of the wound process, the question of the possibility of carrying out autodermoplasty is being considered.

Piogenic trophic ulcers

Piogenic trophic ulcers occur against the background of nonspecific purulent soft tissue diseases (pyoderma, infected wounds, etc.) in patients from socially disadvantaged groups of the population. This type of ulcers can be attributed and long-term healing skin defects that have arisen after a complicated complication of rye, carbuncle, abscess and phlegmon. In its classical version, pyogenic trophic ulcers are multiple superficial purulent foci that have a rounded shape and are covered with a thick purulent coating with a pronounced perifocal inflammatory response. An important diagnostic criterion is considered a syndrome of systemic inflammatory reaction in the absence of signs of defeat of vascular systems of the limb and other causes of ulcer formation. The development of trophic ulcers usually cause Gram-positive cocci Staphylococcus aureus, Streptococcus spp., Much less often - Pseudomonas aeruginosa and other gram-negative rods.

Pyogenic trophic ulcers usually last for a long time, persistently. The main methods of treatment are surgical treatment of purulent foci, antibacterial therapy (protected semi-synthetic penicillins (amoxiclav 625 mg 2 times a day), cephalosporins of II-III generation, etc.), restorative and topical therapy. In the formation of extensive skin defects, the skin is plasticized.

Post-traumatic trophic ulcers

Posttraumatic trophic ulcers are a rather heterogeneous group of chronic skin defects that occur after surgery, various mechanical, thermal, radiation and other skin lesions. In recent years, the incidence of post-injection ulcers of limbs in patients with drug dependence has increased. It is necessary to distinguish between trophic ulcers that have arisen after a sufficiently strong impact of a traumatic agent that caused severe local disturbances of microcirculation, from ulcerative defects that developed after a trauma on the background of venous, arterial, neurologic and other pathologies.

The main method of treatment of posttraumatic ulcers is excision of scar tissue and trophic tissues with skin defect plasty. To close most of the defects use plastic with local tissues, combined methods. If it is necessary to close ulcers on the supporting surfaces of the limb, in the region of the joints, and also in the case of radiation ulcers, the plastic is used with full-layer vascularized flaps, using a dosed stretch of tissues, rotational skin-fascial flaps, Italian skin plasty, Filatov's stem, transplantation of free flaps in the microvascular anastomoses.

Trophic ulcers on the background of malignant neoplasms

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

Such trophic ulcers have uneven, undermined edges, the bottom is deep, crater-like, infiltrated, filled with necroses, abundant fetid detachable. To verify the diagnosis, a histological examination of the biopsy specimens taken from the edges is performed. Treatment of such patients is mainly carried out by oncologists and dermatologists.

The methods of treatment for this vast and heterogeneous group depend on the stage of the malignant disease. In the absence of distant metastasis, extensive excision of the affected tissue with cutaneous plastic surgery of the wound defect or amputation (exarticulation) of the limb, regional lymphadenectomy. In case of complications in the form of bleeding, disintegration of the tumor accompanied by intoxication, palliative interventions in the form of partial or complete removal of the tumor, limb amputation, simple mastectomy are possible. These interventions allow patients to prolong their lives and improve their quality of life.

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

Trophic ulcers on the background of systemic connective tissue diseases

Trophic ulcers on the background of systemic connective tissue diseases usually do not have specific signs. For the recognition of nature, the diagnosis of the underlying disease is of great importance. Purposeful examination of patients should be carried out with prolonged atypical ulceration without a tendency to regenerate, and also in case of syndromes showing systemic autoimmune damage to organs and tissues (polyarthritis, polyserositis, renal, heart, lung, eye, etc.). Trophic ulcers occur against the background of skin syndrome, to some extent present in patients with collagenoses. A skin defect occurs as a result of necrotic vasculitis. More often trophic ulcers affect lower extremities (shin, foot), but atypical localization (hips, buttocks, trunk, upper limbs, head, oral mucosa) is also possible.

Trophic ulcers on the background of other diseases

Some clinical features have trophic ulcers that have arisen against the background of gangrenous pyoderma. Most often they occur in patients with Crohn's disease, ulcerative colitis. Approximately 10% of these patients have gangrenous pyoderma - one of the most severe extraintestinal manifestations. For such ulcers is characterized by the presence of multiple sharply painful purulent-necrotic skin defects, which gradually increase in size. The edges of the trophic ulcer have cyanotic edentulous edges and a ring of hyperemia. Localized trophic ulcers mainly on the feet and legs.

In 30% of patients it is possible to form ulcerative defects on the buttocks, trunk, upper limbs.

Trophic ulcers are distinguished by the persistent flow of lupus erythematosus. With a prolonged I phase of the wound process. Regenerator possibilities are sharply reduced, which is connected both with the course of the underlying disease, and with the standard therapy (corticosteroid hormones, cytostatics, etc.). With the stabilization of the patient's condition with the achievement of stable remission, autodermoplasty not only significantly speeds the healing of extensive ulcerative defects, but also makes this healing the only possible. 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, more rare diseases are detected in no more than 1% of cases, but they cause the greatest difficulties in diagnosis.

Diagnosis of them requires a careful study of anamnesis, recognition of the underlying disease. A special examination should be carried out with prolonged atypical or progressive ulceration without a tendency to regenerate. In doubtful cases biochemical, serological, immunological, histological and other research methods are shown, which allow to reveal the nature of the underlying disease.

Symptoms of trophic ulcers

The most common varicose trophic ulcer. Against the background of compaction and swelling of the tissues, deep and superficial, rounded, oval or polycyclic outlines are formed, ranging in size from 2-3 to 5-10 cm and more. Edges of ulcers are uneven, undercut. They are often localized in the lower third or on the anterolateral surface of the tibia. Trophic ulcers differ torpid current, quite often there is secondary infection (erysipelas or phlegmon). The bottom is covered with serous-purulent discharge, sluggish granulations, accompanied by pain.

Ischemic trophic ulcers have steep, well-defined edges, their bottom is usually covered with a scab, under which tendons can be seen. Separated lean. Other signs of ischemia - lack of hair on the foot and shin, glossy atrophied skin: there is no hyperpigmentation, no sclerosis of the skin and subcutaneous tissue. The bottom is dry - gray or black. When palpation, soreness and absence or loss of pulse on peripheral arteries are noted. Trophic ulcers are often located over the ankles and bony protuberances, on the toes.

With neurotrophic ulcers, the foot skin is dry, warm, there is no sensitivity, and the pulse on the arteries is preserved. Trophic ulcers are deep, often with omozolelems, there is edema caused by sympathetic nerve damage and constant vasodilation. The bottom is dry - gray or black. When palpation, first on the thumbs, and then on the feet, the sensitivity is lost. Later the Achilles reflex and proprioceptive sensitivity disappear. Trophic ulcers are localized on often traumatized, deformable areas of feet, soles, heels and thumb.

Classification of ulcerative-erosive skin lesions by etiology

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

• postthrombophlebitic disease;
• varicose veins;
• congenital venous angiodysplasia, Klippel-Trenone syndrome.

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

• against the background of macroangiopathies:
• obliterating atherosclerosis of the vessels of the lower limbs;
• obliterating thromboangiitis (Buerger-Vinivarter disease),
• postembolic occlusion of the arteries of the lower extremities.
• trophic ulcer against a background of microangiopathies:
• diabetic trophic ulcer;
• hypertensive-ischemic trophic ulcer (Martorel's syndrome).

III. Trophic ulcer caused by arteriovenous fistulas:

• congenital (Parkes Weber syndrome);
• posttraumatic trophic ulcer.

IV. Trophic ulcer against the background of lymphatic outflow:

• primary lymphedema (Milroy's disease, etc.);
• secondary lymphedema (after the transferred face, surgical interventions, radiotherapy, etc.);
• lymphedema on the background of filariasis, etc.

V. Posttraumatic trophic ulcer:

• after chemical, thermal damage and electric injury;
• due to mechanical and gunshot injuries of soft tissues;
• due to human, animal and insect bites;
• osteomyelitic;
• decubital;
• amputation stumps of the foot, shin, thigh;
• postoperative scars (cicatricial and trophic ulcers);
• postinjection;
• beam.

VI. Neurotrophic ulcers:

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

VII. Trophic ulcer arising on the background of common diseases:

• systemic connective tissue diseases and similar diseases and syndromes (rheumatoid polyarthritis, systemic lupus erythematosus, dermatomyositis, scleroderma, nodular periarteritis, Raynaud's disease, Wegener's granulomatosis, Crohn's disease, anti-phospholipid syndrome, cryoglobulinemia, gangrenous pyoderma, etc.) );
• chronic diseases of the cardiovascular system (ischemic heart disease, heart defects, cardiomyopathies, etc.), with severe circulatory failure;
• chronic liver disease, kidney disease;
• severe chronic anemia and other blood diseases (sickle cell anemia, hereditary spherocytosis, thalassemia, etc.);
• endocrinopathy ("steroid" ulcers, etc.);
• metabolic diseases (gout, amyloidosis, etc.);
• beriberi and alimentary depletion.

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

• tuberculosis (condensed erythema Bazena, colliquative skin tuberculosis, scrophuloderma, etc.), syphilitic, leprosy, anthrax, with Lyme disease (borreliosis), sapa, melioidosis, leishmaniasis of the skin (Borovsky's disease), nocardiosis, epithelioid angiomatosis (cat scratch disease) and other;
• erosive-ulcerative lesions of herpes simplex or varicella zoster,
• mycotic (fungous);
• pyogenic, developed in connection with nonspecific infectious diseases of the skin and subcutaneous tissue (phlegmon, erysipelas, pyoderma, etc.).

IX. Trophic ulcers, arising on the background of neoplasms:

• benign skin lesions (papillomas, nevuses, fibroids, etc.);
• malignant neoplasms of the skin and soft tissues (Kaposi's sarcoma and other sarcomas, melanomas, basal cells, etc.);
• blood diseases - ulcerative-necrotic vasculitis (hemorrhagic vasculitis, hemorrhagic purpura of Shenlaine-Genoch, leukemia, fungal mycosis, agranulocytosis, etc.);
• malignant neoplasms of internal organs;
• decay 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 have arisen against a background of acute and chronic skin diseases - eczema, dermatitis, psoriasis, vesicular dermatosis, etc.

XI. Artificial trophic ulcer on the basis of self-mutilation, pathimymia, 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.

[1]

Complications of trophic ulcers

The prolonged existence of a ulcerative defect often leads to various complications, which are considered the main cause of emergency hospitalization of a significant proportion of patients. The main complications include:

• dermatitis, eczema, cellulitis, pyoderma;
• erysipelas, phlegmon, anaerobic infection;
• tendonitis, periostitis, contact osteomyelitis;
• thrombophlebitis; lymphangitis, regional lymphadenitis, secondary lymphedema;
• arthritis, arthrosis;
• tetanus;
• bleeding;
• malignization;
• infection of insect larvae (wound miase).

With inadequate local therapy of ulcers with the use of preparations on an ointment basis, as well as with insufficient hygiene, periulcerous complications in the form of dermatitis, eczema, cellulitis and pyoderma are possible. In this acute inflammation on the skin in the circumference appears diffuse hyperemia, infiltration, moknutie with the development of erosions, pustules. At this stage, the previously used dressings should be discarded and switched to wet-drying dressings with iodophores antiseptics (iodopyron, povidone-iodine, etc.) or absorbent multilayer dressings. Change dressings should be made 1-2 times a day. Glucocorticoid ointments, creams, pastes or talkers containing salicylates (zinc oxide, salicylic-zinc paste), [lotion or ointments (diprosalic, whitewash etc.) are applied to the inflamed skin (but not to the ulcer!)]. The most common skin inflammatory complications occur in patients with venous trophic ulcers located in phase I 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. For erysipelas is characterized by an acute onset with a predominance in the first stages of intoxication symptoms accompanied by chills, high fever, and severe weakness. A little later, there are typical local changes in the form of diffuse hyperemia of the skin with more or less clear boundaries of uneven shape. The skin is infiltrated, edematous, hot to the touch, painful, in the form of a roller rises above the unshaven areas of the skin. Against the background of erythema erythema, there may be discharge surface bubbles with serous exudate. With a more severe course, the appearance of hemorrhages from small petechiae to extensive hemorrhages with the formation of draining bubbles filled with serous-hemorrhagic exudate, develops a ternary lymphangitis in the thigh, inguinal lymphadenitis. The main methods of treating these complications are antibacterial therapy (semisynthetic penicillins, cephalosporins, etc.), adequate local therapy and physiotherapeutic treatment (UFO). Relapses of erysipelas lead to limepodemia of the limb. For the prevention of recurrence of erysipelas, healing of a ulcerative defect (entrance collar of infection) and a monthly appointment of prolonged synthetic penicillins (retarpen or extencellin 2,4 million units) is necessary.

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

Anaerobic clostridial and nonclostridial infections are considered the most serious complication. Most often, it occurs against the background of limb ischemia, inadequate care for ulcerative defect, local application of ointments on a fat basis (Vishnevsky ointment, etc.). The infection develops rapidly, it takes significant limb areas with the development of necrotizing dermatocellulitis, fasciitis and myositis, accompanied by a pronounced systemic inflammatory reaction and severe sepsis. Delayed diagnosis and late hospitalization lead to frequent loss of limb and high lethality, reaching 50%.

In the conditions of a long-term ulcerative defect, the destructive process can spread to the deep layers of soft tissues with the development of tendonitis, periostitis, contact osteomyelitis, purulent arthritis, significantly complicating the possibility of self-healing of a chronic wound.

Bleeding often occurs in patients with chronic venous insufficiency as a result of sarcoid artery erosion located along the edges or in the bottom of a trophic ulcer. Recurrent bleeding often occurs in patients with malignant trophic ulcers or against malignant neoplasms of the skin and soft tissues. The blood loss can be significant, up to the development of hemorrhagic shock. When an arsenic is large enough, and with active bleeding, it is necessary to flash the area of bleeding or ligate the vessel throughout. However, in most cases, for adequate hemostasis, it is sufficient to apply a pressure bandage with a hemostatic sponge, elastic bandage and an elevated limb position. Possible hemostasis with phlebosclerosis therapy.

Malignancy is noted in 1.6-3.5% of cases.

Predisposing to malignancy factors are long periods of the trophic ulcer (usually more than 15-20 years), frequent relapses, inadequate therapy with ointments containing irritants (Vishnevsky ointments, ichthyol, etc.), frequent ultraviolet and laser irradiation of the ulcer surface. Malignancy is suspected in the absence of positive healing dynamics, with rapid progression, the appearance of excess tissue overlying the wound, the appearance of foci of putrefactive destruction of tissues with the appearance of necrosis, fetid detachable, increased bleeding. Verify the diagnosis by conducting a biopsy of various suspicious areas of the edges and bottom.

Many experts do not consider wound miass as a complication, moreover, insect larvae are specially used for carrying out 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.

[2], [3]

How to recognize trophic ulcers?

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

In most cases, the characteristic clinical symptomatology allows us to establish the true cause of education at the first examination of the patient. Diagnosis is based on anamnestic information, the results of the examination of the patient and the area of skin changes, data of instrumental and laboratory methods of investigation. When the diagnosis is made, the clinical signs and features of local lesion that are characteristic of this or that pathology are taken into account. Thus, the detection of an ulcerative defect in the medial ankle, 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 a background of chronic venous insufficiency. The occurrence of an ulcer on the plantar surface of the foot in a patient with impaired skin sensitivity makes it possible to reasonably suspect the neurotrophic genesis of ulcers. In a number of cases, especially with an atypical course of ulcerative lesions, as well as to clarify the nature of the underlying disease, instrumental and laboratory diagnostic methods are needed. In vascular (venous and arterial) lesions, the main diagnostic methods are ultrasound dopplerography and duplex scanning, with osteomyelitis - radiography of bones, caused by malignant neoplasms - cytological and histological methods.

No less important is the evaluation of the ulcerative defect itself with the detailing of its localization, size, depth, stage of the wound process and other parameters that may be specific for the underlying disease, reflect the dynamics and effectiveness of the treatment. For this, a visual assessment of ulcers and surrounding tissues is used with a description of all available changes, planimetric methods, photography and digital photometry.

The size of the ulcer, the depth of the defect, its location, the volume and severity of microcirculatory changes in surrounding tissues, the development of infection are important factors in determining the severity of the disease and its prognosis. The depth and area of skin ulcers can be different. Depending on the depth of tissue destruction associated with the ulcerative process, distinguish:

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

Depending on the size distinguish:

• small trophic ulcer, up to 5 cm2;
• average - from 5 to 20 cm2;
• a large trophic ulcer - from 20 to 50 cm2;
• vast (gigantic) - over 50 cm2.

Prospects for healing ulcerative defect largely depend on the severity of blood flow disorders in the skin located around the ulcer. In some situations, even when the root causes leading to the formation of ulcers are eliminated, irreversible microcirculation disorders develop in the surrounding tissues, which leave no room for self-healing of the skin defect. The main methods for diagnosing microcirculatory disorders are the measurement of transcutaneous oxygen tension, laser Doppler flowmetry and thermometry.

All ulcerative defects are infected. In the case of pyogenic ulcers, the infectious factor is the leading cause of the disease. In the first phase of the wound process, the dynamic evaluation of the inflammatory inflammatory factor is extremely important for the detection of bacterial or fungal pathogens and the selection of targeted antibiotic therapy. To do this, microscopy of the smear is performed, allowing in a short time to determine the composition of microflora and its number, sensitivity to antibiotics. If a malignancy of the ulcer or its malignant nature is suspected, a histological examination of the biopsies taken from the suspicious areas of the margins and the bottom of the ulcer is made. Other diagnostic methods are used according to indications or in case of detection of rare causes of ulceration, which require the use of additional diagnostic methods.

The construction of a clinical diagnosis with trophic ulcer should reflect the features of the course of the underlying disease, its complications according to the international classification of diseases. For example, postthrombophlebitic disease of the lower limbs, recanalized form, chronic venous insufficiency of the VI class, extensive trophic ulcer, dermatitis of the left tibia; or obliterating atherosclerosis of the vessels of the lower extremities, occlusion of the ilio-femoral segment to the right, chronic arterial insufficiency of the fourth degree, trophic ulcers of the rear of the foot; or type II diabetes mellitus, severe course, decompensation stage, diabetic nephropathy, retinopathy, diabetic foot syndrome, neuropathic form, plantar trophic ulcer, left foot left cellulitis.

Differential diagnosis of trophic ulcers

When conducting differential diagnosis, it should be borne in mind that most ulcers of the lower extremities (80-95%) are venous, arterial, diabetic or mixed. Other diseases should be suspected only after exclusion of the main causes or in case of ineffectiveness of standard therapy. One of the main differential diagnostic methods is the determination of pulsation on the arteries of the lower extremities, which must be performed by all patients who have ulcerative defects.

Trophic ulcers should be distinguished from nodular periarteritis, gnarly vasculitis, malignant neoplasms (basal cell and squamous cell carcinoma of the skin, skin lymphomas), injuries, pressure sores, gangrenous pyoderma, etc.

[4], [5], [6]

Treatment of trophic ulcers

Treatment of trophic ulcers is carried out taking into account the principles of therapy of skin diseases. For the treatment of varicose ulcers, therapy of the underlying disease, phlebectomy or daily wearing of elastic stockings is required, to elevate the venous pressure - the elevated position of the legs. Weekly impose a zinc-gelatin bandage. It is necessary to treat the phenomena of dermatitis, eczema in accordance with the manifestations of the skin-pathological process, to remove necrotic tissues. When infected foci prescribe antibiotics of a wide range of action. Apply skin transplantation.

To treat ischemic ulcers, drugs that improve blood flow in the arteries, treat arterial hypertension. For a radical cure reconstructive surgery on the arteries is used.

Trophic ulcers in a patient with idiopathic progressive atrophy of the skin.

In the treatment of trophic ulcers, special attention should be paid to the use of vitamin, antihistamine, biogenic stimulants. Inclusion of phlogenzim (2 capsules 3 times a day) significantly increases the effectiveness of treatment.

With long-term non-healing trophic ulcers, it is recommended to prescribe corticosteroids inside at low doses (25-30 mg per day). Widely used physiotherapeutic procedures (helium-neon laser, UFO, ion-galvanization with zinc, local mud baths, etc.), externally - products that improve trophism of tissues (solcoseryl, actovegin, etc.), which contribute to the epithelization of ulcers.

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