Diabetic foot: causes, symptoms, treatment methods

Charcot's foot is one of the dangerous complications of diabetes mellitus, which can lead to serious consequences or disability for the patient.

This syndrome includes a combination of many factors affecting the tissues of the foot, including damage to the nervous system, blood vessels, and bones.

The development of diabetic foot syndrome in the form of Charcot's foot is accompanied by subluxations or dislocations of the joints of the foot, local inflammation with destruction of bone tissue, bone fractures, neuropathy - a pathology of the nervous system that leads to loss of sensitivity.

Doctor of Medical Sciences Maxim Nikolaevich Kudykin noted that this complication has become more common. Despite the fact that the complication is severe, patients seek help in the later stages of the disease. Often they do not feel pain.

It is noted that with this syndrome, trophic ulcers develop on the patient’s legs.

A similar condition was first described in 1703 by the English physician Mitchell. The syndrome is named after the French neurologist Charcot, who described in detail the relationship between neuropathy and damage to the ankle joint. This condition can occur with syphilis, leprosy, and alcoholism. Modern researchers have found that the syndrome most often develops in patients with diabetes.

Currently, statistics on this complication have been collected. Diabetic osteoarthropathy develops in approximately every two hundred patients with diabetes, and in every third patient with diabetic neuropathy.

If in early studies it was noted that this was a fairly rare complication, then with the spread of diabetes mellitus in developed countries, this complication began to be detected more often.

Etiology and pathogenesis

The universal trigger for the development of DOAP is hyperglycemia, which leads to the development of neuropathy, which causes a whole cascade of pathological processes, the outcome of which may be DOAP.

Despite the fact that DOAP was described more than a hundred years ago, its pathogenesis remains unclear. There are currently 3 leading theories:

• neurotraumatic states that the sensory form of distal neuropathy leads to decreased sensitivity and an increased likelihood of undetected foot injury and pathological expansion of range of motion in the joints. While motor neuropathy causes atrophy of the interosseous muscles, gait disturbances and the development of foot deformities with the formation of abnormally loaded areas of the foot, predisposing to injury to the musculoskeletal system [36];
• neurovascular , according to which, when autonomic nerve fibers are damaged, there is a disruption of the innervation of the vascular system, an increase in the number of arterio-venous shunts with an increase in local volumetric blood flow in the bone tissue of the feet and, as a consequence, its demineralization with subsequent destruction due to injury. However, to date, the relationship between increased blood flow to the bones of the feet and their resorption has not been fully determined [9,13];
• the combined one is modern and combines the two hypotheses described above with the inflammatory theory (Fig. 3) [34].

It is known that the risk of developing DOAP increases with increasing duration of diabetes, while no differences by gender and age have been identified; the process can accompany decompensation of diabetes, regardless of the type of diabetes, and is more often unilateral, but in 9-25% of cases bilateral damage is observed [4 ]. Most patients indicate a history of minor foot injuries; some have a history of infected ulcers, osteomyelitis, or surgical interventions for this reason. There are rare cases of the development of DOAP after successful revascularization of the arteries of the lower extremity [16].

Thus, DOAP occurs in patients with the above risk factors and is an uncontrolled inflammation in the skeletal system of the foot, leading to osteolysis with subsequent destruction and dislocation of the bones of the foot [21].

Angiopathy

In diabetes, damage to blood vessels often occurs - angiopathy. They become covered with atherosclerotic plaques, which leads to circulatory failure in the foot. It looks a bit like rusty pipes. Very little water comes out of the tap due to rust blocking the inside of the pipes. The same thing happens when blood vessels are clogged. If the vessels in the legs become clogged or completely blocked, the skin and tissues will suffer first from poor circulation. The process of delivering oxygen and nutrients to the limb will be disrupted, which means cell death in the affected area.

• Decreased ability to fight infection
• The ability to heal wounds will decrease.
• Signs of blood vessel damage
• Pain in the lower leg when walking,
• A change in the normal color or temperature of the feet,
• Leg pain at night or while resting.

If nerve damage is combined with poor circulation, the risk doubles. You are more likely to get injured (because you don't feel pain) and the injury will lead to infection or ulceration. Healing will not occur due to poor circulation, which will inevitably lead to gangrene.

Risk factors for developing diabetes include poor diet and glucose control, poor circulation, smoking, and diabetes mellitus of more than 10 years.

Uncontrolled inflammation

Bone fracture is known to release proinflammatory cytokines, tumor necrosis factor-α and intelekin-1β, which increase the expression of receptor activator of nuclear factor-κB ligand (RANKL) polypeptide from local cells. RANKL activates the transcription of nuclear factor-κβ (NF-κβ), which in turn stimulates the maturation of osteoclasts from progenitor cells, thereby increasing bone resorption and loss.

At the same time, NF-κβ stimulates the production of the glycopeptide osteoprotegerin (OPG) from osteoblasts, an effective antagonist of RANKL [12,27]. However, recent genetic studies in patients with DOAP have identified single polymorphisms in the OPG gene, contributing to changes in the OPG/RANKL ratio and, as a consequence, an imbalance in bone remodeling towards increased resorption [25,31].

Due to the fact that, against the background of diabetic neuropathy, a fracture of the foot bones occurs without serious pain and the patient continues to walk, repeated injuries to the affected limb occur. This leads to the constant production of pro-inflammatory cytokines, which in turn support osteolysis, completing a vicious circle [21].

In addition, peptides released from nerve endings, in particular those associated with the calcitonin gene (cocalcigenin, calcitonin gene-related peptid - CGRP), play an important role in the pathogenesis of DOAP, since it is known as a RANKL antagonist. Thus, the decrease in CGRP due to nerve damage also leads to strong expression of RANKL [22 ].

A number of researchers talk about the role of osteopenia in the development of DOAP and a higher incidence of osteopenia in patients with type 1 diabetes, although the incidence of DOAP is the same in type 1 diabetes and type 2 diabetes. Some studies have shown a higher incidence of systemic manifestations of osteopenia, in particular in the femoral neck in patients with type 1 diabetes, than locally in the feet [18,30].

Factors in the development of DOAP also include osteopenia due to insulin deficiency, conditions associated with vitamin D deficiency with or without renal failure and secondary hyperparathyroidism, when taking thiazolidinediones for type 2 diabetes and glucocorticoids as immunosuppressants in people who have had a kidney transplant and/or pancreas [26]. It is known that increased formation of advanced glycation end products, reactive oxygen species, and lipid oxidation during chronic hyperglycemia can also increase RANKL expression [22].

Diabetic foot symptoms. Stages of the disease.

People with diabetes need to be as attentive and scrupulous as possible to their own health. At the first changes in your health and well-being, it is advisable to consult a specialist. Feet are a part of the body that also requires increased attention.

It is recommended to consult your doctor if the following symptoms occur:

· feeling of goosebumps in the legs

Numbness of the lower extremities, tingling

burning sensation in the legs

the appearance of cramps in the calves

hair loss in the shin area

· appearance of pigmentation on the legs or changes in color (blanching, redness, blueness)

darkening of the nail plate (bruising under the nail plate)

formation of cracks in the feet

formation of weeping eczema between the fingers (small blisters with clear liquid inside)

· injuries on the legs heal slowly or do not heal at all

· appearance of itching

formation of edema

peeling, dry skin

Symptoms of DFS may also include increased fatigue, as well as pain in the legs at night and during walking.

Clinical picture

DOAP can be encountered in the practice of a doctor of any specialty (surgeon, traumatologist, endocrinologist), but sometimes its diagnosis is difficult.

The first clinical signs of DOAP are swelling, hyperemia and local hyperthermia of the foot (Fig. 4).

It is important to know that due to the presence of severe diabetic neuropathy in patients and a significant decrease in peripheral sensitivity, pain syndrome may be absent, however, the presence of any pain is noted in 75% of patients, it is also possible to have a feeling of discomfort, unpleasant sensations when loading the limb (a feeling of “crunching”) "in the foot, "dip" while walking). Body temperature usually does not increase. Pathological mobility, crepitus of bone fragments and deformation of the foot may appear, which is manifested by a slight change in the configuration of its inner edge.

In the absence of adequate immobilization, a disruption of the normal anatomy and biomechanics of the foot occurs - the formation of more pronounced deformation of the foot, in typical cases - flattening of its arch.

Over time, the fracture heals with the formation of a callus. If treatment is not started in a timely manner or the patient’s low adherence to it, severe uncorrectable deformities of the foot develop, most often of the “paperweight” or “rocker foot” type. This is accompanied by valgus deformation of the inner edge of the foot in the tarsal area, hammertoe or claw-shaped deformity of the toes, as a result the foot loses mobility and supporting ability (Fig. 5) [6,8].

Against the background of deformation, areas appear on the foot that are overloaded during walking, and therefore the risk of formation of ulcerative defects increases, which, if infected, may lead to the development of purulent-necrotic complications (phlegmon, osteomyelitis and gangrene) (Fig. 6).

Classification used for Charcot arthropathy

According to the clinical manifestations of the disease, the course of DOAP has recently been divided into two stages: acute (approximate duration is 6 months) and chronic (occurs after the end of the acute stage).

The most commonly used anatomical classification was developed by L. Sanders and R. Frykberg in 1991.

Anatomical classification of Charcot's foot (Sanders LJ and Frykberg RG, 1991)

• I – metatarsophalangeal joints;
• II – tarsometatarsal joints;
• III – tarsal joints;
• IV – ankle joint,
• V – calcaneus. (+ frequency of occurrence)

*Sanders L, Frykberg R. Diabetic neuropathic osteoarthropathy: The Charcot foot. In: Frykberg RG, editor. The high risk foot in diabetes mellitus. 1991. p.325-333.

The radiological classification is based on the work of S. Eichenholtz, who in 1966 described changes in the osteoarticular structure of the foot with DOAP in the form of a three-step process:

Phase I (development) is characterized by acute destruction of the joint with subchondral fragmentation, diffuse osteopenia, ligament distortion and subluxations;

in phase II (consolidation), resorption of most bone fragments occurs and their consolidation with the underlying bone, which partially stabilizes the skeleton of the foot;

Phase III (reconstruction) is characterized by bone remodeling processes, subchondral osteosclerosis and the formation of osteophytes.

Pathoanatomical classification of Charcot's foot (Eichenholtz SN, 1966)

0) Bone marrow edema 1) Fragmentation stage 2) Fusion stage 3) Restructuring stage

*Eichenholtz SN. Springfield (Ill): Charles C. Thomas;. 1966.

Modified by Sella E. J. and Barrette C. (1999)

0) Pain, swelling, hyperemia and hyperthermia over the joint; 1) Osteopenia, subchondral cysts, erosions, diastasis; 2) Subluxations; 3) Dislocation and destruction of the joint; 4) Healing and bone hypertrophy.

*Sella EJ, Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg. 1999;38(1):34-40. doi: 10.1016/s1067-2516(99)80086-6.

Anatomical classification (Brodsky JW)

Lisfranc region

Chopard and subtalar joint area

Ankle joint. Posterior heel

Combined lesion Anterior section.

*(Brodsky JW, Philadelphia: Mosby Elsevier, 2007:1333)

Clinical classification of Charcot foot (Rogers L., 2012)

A) Without deformation B) Charcot with deformation C) With deformation and wound D) With osteomyelitis

*Rogers LC Diabetes Care. 2011; 34(9):2123-9. doi:10.2337/dc11-0844

Diagnostics

If a patient with diabetes develops unilateral swelling of the foot, especially if the skin is intact, taking into account the above risk factors (long-term course of diabetes, severe diabetic neuropathy, etc.), DOAP should first be excluded.

Often the clinical picture of DOAP can be regarded as phlegmon, deep vein thrombosis, gouty arthritis, which requires high-quality differential diagnosis to ensure correct treatment and prevention of irreversible disability of the patient.

The diagnosis is based on a comprehensive assessment of the clinical picture, anamnesis and examination, which includes an assessment of the state of the nervous, vascular systems and the musculoskeletal system of the lower extremities.

In most patients with DOAP, using neurological instruments (tuning fork, monofilament, neurological needle, tip-therm) and Doppler ultrasound, distal sensory-motor neuropathy with preserved or increased arterial blood flow in the feet is detected.

An important component of the objective diagnosis of DOAP and assessment of the activity of the process during treatment is skin thermometry, which is carried out using a household infrared thermometer according to the protocol at symmetrical points on both feet. A difference in skin temperature of more than 2°C compared to the contralateral limb indicates the acute stage of DOAP [8,10] .

Radiography is the main method in the primary diagnosis of osteoarticular changes; in addition, it is an easily accessible and inexpensive study that visualizes the structure and degree of bone mineralization. Unfortunately, radiography is not always informative, especially with regard to microfractures and dislocations in the early stages of DOAP (X-ray negative stage). In this regard, in the presence of clinical signs of DOAP and a normal radiographic picture, it is recommended to use magnetic resonance imaging (MRI). The advantage of MRI over radiography is its unique ability to visualize soft tissue, which allows diagnosing DOAP already at the stage of formation of bone marrow edema, intraosseous cysts and microfractures, as well as differential diagnosis between osteomyelitis and ostearthropathy [28].

Computed tomography (CT), unlike MRI, does not show the condition of the bone marrow, but more clearly than radiography, it reveals fractures at the stage of periosteal reaction, and three-dimensional reconstruction of CT images allows you to observe the healing process and accurately determine the degree of displacement of the bones relative to each other, which may be required when planning reconstructive surgery on the foot (Fig. 7) [8].

Among the methods of radiation diagnostics, bone scintigraphy with technetium-99m is of interest, sensitive to active bone pathology, but it must be remembered that a decrease in microcirculation can lead to false-negative results, and in the presence of osteomyelitis, differential diagnosis with DOAP is impossible without labeled leukocytes, which shows the low specificity of this method. Some studies have shown the effectiveness of positron emission tomography (PET) in the differential diagnosis of osteoarthropathy and osteomyelitis. However, PET is not widely available both in Russia and abroad [20,24].

Description of the manifestations of “Diabetic foot”

Diabetic foot syndrome (diabetic foot or DFS) is a complex of complications of diabetes mellitus. This is a dangerous disease that develops in people with diabetes and involves the process of damage to the epidermis, dermis, bones, and nerve endings on the feet; With untimely or absent treatment, loss of a leg is possible.

According to statistics, every tenth person diagnosed with diabetes mellitus is diagnosed with diabetic foot disease; 50% of diabetics are at risk.

Diabetes mellitus implies a malfunction in the functioning of the nervous and vascular systems, which leads to disorders associated with blood supply and nervous regulation of the limbs. These violations are the cause of the disease DFS.

In the initial stages, the main symptoms of the disease are superficial ulcerative lesions on the feet; in later stages, the ulcers penetrate deeper, affecting the muscles, tendons, and bones. In the final stages, limited and then extensive gangrene forms.

The main methods of treating diabetic foot are normalization of blood sugar, local treatment of the skin and nail plates, drug therapy, and surgical measures.

Diabetic foot belongs to the category of those diseases whose treatment absolutely cannot be delayed! Gangrene, general blood poisoning, amputation, death of the patient - these are the real consequences of inaction. Therefore, you should contact specialists immediately.

Treatment

Comprehensive treatment of DOAP should be aimed at unloading the affected limb, restoring bone tissue and preventing further fractures of the foot bones [17].

Due to the variety of etiological factors of increased bone resorption, local and/or systemic osteoporosis in patients with DOAP and the insufficient number of prospective randomized placebo-controlled studies in this area, treatment principles are largely based on expert opinion rather than on high-level clinical evidence.

It has been proven that unloading the foot in the active stage of DOAP is the most effective component of treatment and is aimed at preventing the progression of the deformity. The ideal method of immobilization is considered to be a non-removable individual unloading bandage (IRP) made of Total Contact Cast (TCC) polymer materials similar in properties to gypsum (Fig. 8).

The advantages of polymer dressings include ease of application, lightness, strength, moisture resistance, and air permeability. In addition, the flexible fixation material Softcast™ allows for semi-rigid immobilization [7].

While wearing a non-removable IRP, a decrease in the swelling of the limb is noted within the first days. In the future, in order to prevent “scuffs,” erosions and ulcers of the skin under the IRP while reducing swelling, it must be changed once every 3-4 weeks. The risk of complications is minimized if medical personnel are professionally trained in the manufacture of IRP.

When wearing an IRP, the patient is advised to use bed rest, crutches or a wheelchair if possible to avoid overloading the healthy foot. Immobilization of the limb continues until swelling, hyperemia disappears, the temperature of the skin of the affected foot decreases (the difference with the contralateral limb should be less than 20C) and consolidation of bone fragments is confirmed by radiological or MRI. In most cases, the duration of treatment is at least 5-7 months, sometimes up to 1 year [10].

An alternative method of unloading the limb in the acute stage of DOAP may be a removable, adjustable high orthosis, especially if the heel bone or bone structures of the ankle joint are affected. However, it must be remembered that the effectiveness of immobilization is much lower if the patient has the opportunity to remove the unloading device at home; this often prolongs the treatment period and can lead to unwanted deformations of the foot, therefore the patient is discussed with the rules for using a removable bandage and specially developed instructions are issued [9] .

It must be taken into account that long-term immobilization, in addition to the obvious benefits for DOAP, has disadvantages: it helps to reduce muscle tone and bone mineral density of the limb, as well as joint stiffness. Therefore, when a clinical effect is achieved, before switching to specialized shoes, it is advisable to prepare the patient; for this, ankle bandages made of knitted fabric are used (Fig. 9).

If a patient has foot deformities, complex orthopedic shoes with internal relief that follows the abnormal shape of the foot are needed. Constantly wearing correct orthopedic shoes prevents the development of trophic ulcers in areas of high pressure in people who have undergone DOAP.

In parallel with unloading the limb, correction of glucose-lowering therapy is indicated to achieve compensation for carbohydrate metabolism [6].

The use of antiresorptive drugs is recommended as a pathogenetic treatment for acute DOAP, but to date there is insufficient evidence of effectiveness, since oral and parenteral forms of bisphosphonates and calcitonin have been studied in a few small randomized or retrospective studies. There is convincing evidence that calcitonin has a safer profile in chronic renal failure compared to bisphosphonates [11]. The recently released tumor necrosis factor antagonist drugs α (infliximab, etanercept) and RANKL (denosumab) can potentially also be included in the complex therapeutic treatment of DOAP, but the question of the advisability of their use and dosage regimen requires further randomized placebo-controlled multicenter studies.

There is limited data regarding the effectiveness of ultrasound and electrical bone stimulation. Positive results have been obtained in a small number of patients using these methods in the treatment of DOAP. However, no follow-up studies have been conducted and at present stimulation can only be recommended as an additional therapy in the postoperative period [19,29,35].

Considering the presence of preserved or increased arterial blood flow in the feet in patients with DOAP, the prescription of any vasoactive drugs (pentoxifylline, prostaglandins) is not only not required, but also unacceptable, as it leads to aggravation of the pathological process.

Diabetic osteoarthropathy

What is Charcot's foot? What is the difficulty in diagnosing diabetic osteoarthropathy?

Diabetic osteoarthropathy (PDA, Charcot foot, Charcot joint) is a rare but extremely severe complication of diabetes mellitus, which, if not adequately treated, leads to irreversible disability. This complication can be called one of the most mysterious forms of diabetic foot syndrome, since it is extremely difficult to predict the development of PDA and identify risk groups among patients with diabetes. This complication of diabetes is encountered by doctors of different specialties - surgeons, endocrinologists, orthopedists, but it is not always recognized in time.

The current definition of diabetic osteoarthropathy is “non-infectious bone and joint destruction caused by diabetic neuropathy” [1].

Destructive osteoarthropathy was described in the 19th century by the French neurologist Charcot [2], but not in diabetes mellitus (in the pre-insulin era, late complications of diabetes were practically not encountered), but in syphilitic lesions of the spinal cord pathways (tabes dorsalis). Subsequently, it was found that similar changes in the joints of the feet also occur in various diseases leading to impaired innervation of the lower extremities (syringomyelia, diabetic polyneuropathy, etc.). Currently, the most common form of osteoarthropathy is diabetic.

The prevalence of this complication among patients with diabetes is less than 1% [3], although in the literature there is data on damage to the bone tissue of the feet in 0.1-55% of patients [4]. This inconsistency of information is obviously associated with differences in examination methods and different criteria for diagnosing osteoarthropathy.

Localization of lesions

In the vast majority of cases, PDA affects the bones and joints of the feet. In 1991, a classification of PDA was proposed [3] depending on the localization of the process (Fig. 1). In 20-25% of patients, PDA affects both feet, but usually not at the same time. There are cases of PDA with damage to other joints: the knee and even the elbow.

Etiology, pathogenesis and natural history of PDA

Osteoarthropathy is essentially a lesion of bone tissue, in contrast to typical forms of osteoporosis, which are exclusively local in nature. The cause of such bone damage is a violation of the innervation of the lower extremities due to diabetic neuropathy.

For a long time, the development of PDA was considered mainly from the perspective of neurotraumatic and neurovascular [5]. According to the first, motor and sensory (through the loss of proprioceptive reflexes) forms of neuropathy lead to disturbances in the biomechanics of the foot. The result of this is an abnormal load on individual joints of the foot when walking, leading after some time to their destruction. An alternative theory is based on the discovery of signs of arteriovenous shunting of blood through the vascular bed of bone tissue in PDA, which led to the conclusion about the leading role of abnormal increased blood flow in bone tissue in the development of local osteopenia [6]. In 1989, scientists hypothesized that both recurrent foot trauma and increased blood flow to bone tissue play a role in the development of PDA. Thus, both of these pathological processes are reflected in the “synthetic” theory [7].

It is known that PDA does not develop in patients with circulatory disorders of the lower extremities. This is explained by the fact that with ischemic and neuroischemic forms of diabetic foot syndrome, an abnormal increase in blood flow in bone tissue is impossible.

Despite the fact that the fact that PDA develops only in severe diabetic neuropathy is well known, it is almost impossible to predict the development of PDA, since this complication does not occur in all patients, even with severe neuropathy. In this regard, it has been suggested that PDA is not caused by any form, but only by certain “subtypes” of neuropathy. In 1992, British researchers put forward a hypothesis (later confirmed in a number of studies) that PDA is caused by a special form of diabetic neuropathy with predominant damage to myelinated nerve fibers and the relative preservation of non-myelinated nerve fibers, which causes a violation of microvascular tone, which entails increased blood flow in bone tissue [ 8].

These pathological processes serve as a prerequisite, a kind of background, for the manifestation of PDA - osteoporosis of the distal parts of the lower extremities, which reduces the resistance of the bone to damaging influences. In this situation, a provoking factor (minimal trauma while walking or surgery on the foot) leads to damage to the bone or increased blood flow in it, activation of osteoclasts and “triggers” a rapid and non-stop process of osteolysis, which in the absence of treatment leads to destruction of the foot skeleton.

After the manifestation of PDA, the process goes through four stages [4].

The first (acute) stage is characterized by swelling of the foot, moderate hyperemia and local hyperthermia (Fig. 2). Pain and fever are uncharacteristic. X-ray may not reveal destructive changes (at this stage they are represented only by microfractures); Osteoporosis of the foot bones is detected.

Second (subacute): bone fragmentation and the onset of foot deformation. In typical cases, the arch of the foot flattens on the affected side (Fig. 3). Swelling and inflammation decrease at this stage. X-rays reveal fragmentation of bone structures.

Third (chronic): severe deformation of the foot, the presence of spontaneous fractures and dislocations. The type of deformation depends on the location of the lesion. In typical cases, loads on the foot when walking lead to deformation of the “paperweight” or “rocker foot” type (Fig. 4). This is accompanied by valgus deformation of the inner edge of the foot in the tarsal area and beak-shaped deformity of the toes. X-ray revealed bone fragmentation, severe skeletal deformation, periosteal and paraosseous calcification (Fig. 6). The function of the foot skeleton is completely disrupted; in severe cases, the foot can be figuratively compared to a “bag of bones.”

Fourth (stage of complications): overload of individual areas of the deformed foot leads to the formation of ulcerative defects (Fig. 5); when they become infected, phlegmon of the foot, osteomyelitis, and gangrene may develop.

Diagnostics

Due to the complexity of treating PDA, and also due to the fact that this condition is quite rare in the population, patients with suspected PDA should be referred to specialized departments for diagnosis and treatment (.

PDA is diagnosed based on the clinical picture, medical history (minor trauma, surgery) and radiological signs corresponding to a particular stage. Very often, due to insufficient awareness of general practitioners about PDA, this complication is mistakenly diagnosed as lymphostasis, thrombophlebitis, phlegmon of the foot, etc.

The differential diagnosis is most difficult in the acute stage, when untimely initiation of adequate treatment leads to irreversible disability.

Differential diagnosis of PDA in the acute phase includes two main questions:

• Are inflammatory changes a consequence of damage to bone structures or should they be considered as a manifestation of another disease (phlegmon of the foot, acute thrombophlebitis, gouty arthritis, rheumatic joint lesions, etc.)?
• If there are radiographic signs of bone destruction, is it non-infectious (PDA) or infectious (osteomyelitis) in nature?

To solve the first question, radiographic data of the feet are needed (although in the acute phase only nonspecific changes in the form of osteoporosis may be present). Magnetic resonance imaging and scintigraphy of the foot skeleton reveal microfractures, inflammatory changes, and increased blood flow in the affected bones.

It is possible to evaluate biochemical markers of bone tissue breakdown (hydroxyproline, deoxypyridinoline, collagen fragments, etc.). For a similar purpose, markers of bone tissue remodeling that reflect the activity of osteoblasts (that is, osteosynthesis) can be used - bone isoenzyme alkaline phosphatase, etc. But the level of these substances largely depends on the activity of bone tissue breakdown processes in the skeleton as a whole.

It is obvious that changes characteristic of other diseases: signs of acute thrombophlebitis on ultrasound examination of the venous system, a typical clinical picture of gouty arthritis (with pain and fever, corresponding x-ray and biochemical picture) and others - make the diagnosis of PDA less likely.

For other cases, the most acceptable algorithm for diagnosing PDA in the acute phase today can be considered the following [9]:

Clinical data - suspicion of OAPR X-ray of the foot with negative results Scintigraphy with 99mTc confirmation of the diagnosis MRI and/or repeat radiography (“targeted”, with examination of a specific “area of ​​interest”)

If a patient with diabetes mellitus has unilateral swelling of the foot (especially if the skin is intact), the possibility of PDA must be excluded. If a PDA is suspected and there is an increased risk of its development (long-term diabetes mellitus, severe diabetic neuropathy), it is more advisable to prescribe treatment immediately than to observe irreversible deformation of the foot after a few months.

The second question more often arises in the presence of a trophic foot ulcer or in the postoperative period after amputation within the foot or other surgical intervention. This is due to the fact that osteomyelitis in diabetic foot syndrome is most often secondary, being a complication of a trophic ulcer or wound process. Blood test data help in resolving this issue: neutrophilic leukocytosis is characteristic (although not necessary) for osteomyelitis, but not for PDA. Osteomyelitis is also indicated by some radiological signs (reaction of the periosteum), as well as the presence of a fistula, probing of bone structures at the bottom of the wound. An effective but inaccessible research method is skeletal scintigraphy with the introduction of radioactively labeled leukocytes. The “gold standard” in determining the nature of bone tissue destruction is a bone biopsy.

Treatment of PDA

In the acute phase, the goal of treatment is to stop the processes of osteolysis, prevent pathological fractures or their consolidation.

The most common mistake is prescribing vasoactive drugs. These drugs are not indicated for all forms of diabetic foot syndrome (only for ischemic and neuroischemic), and in case of PDA they can increase the already excessive blood flow in the bone tissue.

The basis of treatment for PDA in the acute stage is complete unloading of the limb until signs of inflammation (edema, local hyperthermia) disappear. Adequate unloading ensures consolidation of bone fragments and is more important than drug treatment [3]. If unloading is not carried out, displacement of bone fragments and the development of progressive foot deformity, shown in Fig. 2-5. In the first days and weeks of the disease, strict bed rest is indicated. In the future, walking is possible, but only in a specially made orthosis, which transfers a significant part of the load from the foot to the lower leg. Temporary unloading during the manufacture of the orthosis can be performed using a splint, which differs from the orthosis in its standard shape (sold ready-made) and less tightly fixing the limb.

After the swelling resolves (usually after 4 months), wearing an orthosis is gradually abandoned, and the patient is allowed to walk in individually made orthopedic shoes (Fig. 7).

The standard method of unloading a limb with a PDA in most foreign countries, especially English-speaking ones (USA, UK, Australia, etc.), is the use of fixing bandages made of polymer materials with properties similar to plaster (Total Contact Cast). But even with highly qualified personnel performing this procedure, the method is fraught with the development of skin lesions (bedsores) under the immobilizing bandage in 10% of cases.

In the acute phase of PDA, medications that affect bone metabolism are used.

Bisphosphonates and calcitonin inhibit the process of bone tissue resorption.

The domestic first-generation bisphosphonate xidifon (etidronate) has an affordable price. 15-25 ml of the prepared solution is prescribed on an empty stomach in intermittent courses (for example, the first 10 days of each month), since its constant use creates a risk of osteomalacia. Modern bisphosphonates - Fosamax (alendronate) and others - are used continuously and are more effective. The dose of Fosamax is 10.0 mg (one tablet) on an empty stomach daily. There are reports of intravenous use of bisphosphonates [Bonefos (clodronate)] for PDA.

Calcitonin (miacalcic) is administered subcutaneously or intramuscularly at 100 IU once a day (usually 1-2 weeks), then as a nasal aerosol at 200 IU daily.

Bone formation is stimulated by active metabolites of vitamin D3 (alpha D3-Teva, etc.) and anabolic steroids.

Alpha D3-Teva is used at 0.5-1 mcg/day (2-4 capsules) after meals. Alpha D3-Teva helps improve calcium absorption in the intestine and activate bone remodeling processes, has the ability to suppress elevated levels of parathyroid hormone, enhance neuromuscular conduction, reducing the manifestations of myopathy. Long-term therapy with Alpha D3-Teva helps reduce pain, increase muscle strength, coordination of movements, and reduce the risk of falls and bone fractures. The incidence of adverse reactions during long-term therapy with Alpha D3-Teva remains low.

Anabolic steroids (retabolil, nerobol) are prescribed by injection once a week for 3-4 weeks.

Calcium preparations do not have an independent effect on bone tissue metabolism, since the inclusion of calcium in bone tissue is regulated by appropriate hormones. These drugs are used as auxiliaries to ensure sufficient calcium intake in the treatment of bone tissue pathology (which should be 1000-1500 mg/day, taking into account all foods). Lactate and calcium carbonate have the greatest bioavailability. They are included in the preparations calcium-Sandoz forte, Vitrum-calcium and calcium-D3-Nycomed, which can be prescribed one tablet per day (about 500 mg of elemental calcium). The last of these drugs also contains vitamin D3, but in prophylactic doses, so this drug should be considered primarily as a source of calcium. Calcium supplements are taken in the afternoon, as this is when their maximum absorption occurs. Calcium gluconate (100 mg tablets) is inexpensive, but has low bioavailability, which is why the required daily dose of the drug is 10 tablets.

Calcitonin and bisphosphonates can cause hypocalcemia, vitamin D3 and calcium supplements can increase calcium levels in the blood. Therefore, it is necessary to determine the level of ionized calcium before the start of treatment and monthly during treatment (in modern laboratories this indicator is determined in capillary blood). Usually a combination of any of the resorption inhibitors, vitamin D3 and calcium supplements is used. Depending on the level of ionized calcium, the doses of certain drugs are increased or decreased. The duration of treatment is 4-6 months.

Auxiliary agents (NSAIDs, elastic bandaging of the limb, sometimes diuretics) are used to eliminate swelling.

X-ray therapy of the affected joints allows you to quickly stop inflammatory phenomena. However, according to a number of placebo-controlled studies, the fact of improvement in the prognosis of PDA after X-ray irradiation has not been confirmed. Therefore, radiotherapy should only be used in combination with adequate unloading of the limb.

The optimal outcome of treatment initiated in the acute phase is the prevention of fractures or consolidation of fragments. The results of treatment can be judged by changes in the clinical picture and control radiography 4-6 months after the manifestation of the disease.

After the inflammatory phenomena subside, an increased risk of PDA remains (in the same or other areas). In addition to general preventive measures (see below), it is advisable to wear orthopedic shoes that reduce the load on the joints of the foot (primarily the tarsus) when walking.

If the process is at the second or third stage, the main goal of treatment is to prevent complications of PDA. If there are foot deformities, complex orthopedic shoes with internal relief that follows the abnormal shape of the foot are needed. A rigid sole with a so-called roll - a raised front part - prevents further displacement of bone fragments when walking. Constantly wearing high-quality orthopedic shoes prevents the development of trophic ulcers in areas of high pressure. Attempts at orthopedic correction of deformities in PDA (arch supports, etc.) are futile and are fraught with the rapid development of ulcers.

Methods of surgical restoration of the foot skeleton in PDA

A number of surgical intervention methods have been proposed aimed at correcting foot deformity in PDA (arthrodesis, resection of bone structures that create increased pressure on the plantar surface and lead to the formation of a non-healing ulcer), but in Russia there is little experience in their use. An undoubted condition for the use of these methods is the complete subsidence of the inflammatory process and osteolysis (since otherwise, surgical intervention may contribute to the emergence of new foci of destruction). It is likely that treatment with drugs that strengthen bone tissue creates more favorable conditions for surgery. However, the issue of indications for surgical treatment and its safety in PDA still remains controversial. Most often, the indication for such treatment is severe foot deformation, which makes it impossible to manufacture adequate orthopedic shoes. In any case, after surgery, it is necessary to ensure a complete 3-month unloading of the affected limb (bed rest, hereinafter referred to as Total Contact Cast or its equivalent) [3].

Prevention of PDA

The issue of prevention methods in risk groups has not been completely resolved. Timely detection of osteopenia in the distal extremities would allow restoration of bone density with the help of appropriate drugs. However, osteoporosis of the foot skeleton on radiography in diabetic patients occurs tens of times more often than PDA, and therefore the group of patients with indications for preventive treatment becomes unreasonably large. In addition, methods for quantitative assessment of bone density (densitometry) of the foot skeleton have not been sufficiently developed, without which it is impossible to get an idea of ​​changes in bone density during treatment, as well as to select the most effective drugs, etc.

Consequently, the basis for the prevention of PDA remains adequate treatment of diabetes mellitus, selected taking into account modern recommendations: teaching patients methods of self-control, maintaining glycemia at a level close to “non-diabetic”, and timely administration of insulin for type 2 diabetes.

Literature

1. International Working Group on the Diabetic Foot. International Consensus on the Diabetic Foot., 1999.
2. Charcot JM Sur quelques arthropathies qui paraissent dependre d'une lesion du cerveau ou de la moelle epiniere // Archives Phisiologie Normale et Patologie. 1868. V. 1. P. 161-178.
3. Frykberg R., Mendeszoon E. Management of the diabetic Charcot foot Diabetes // Metabolism research and reviews. 2000. V. 16 (Suppl. 1). P. S59-S65.
4. Dedov I. I., Antsiferov M. B., Galstyan G. R., Tokmakova A. Yu. Diabetic foot syndrome. M.: Federal Diabetology Center of the Ministry of Health of the Russian Federation, 1998.
5. Bradshaw TW Aetiopathogenesis of the Charcot, vol. foot: an overview//Practical Diabetes International. January-February 1998. V. 15. No. 1. P. 22-24.
6. Boulton AJM, Scarpello JHB, Ward JD Venous oxygenation in the diabetic neuropathic foot: evidence of arterial venous shunting? // Diabetologia. 1982. V. 22. P. 6-8.
7. Banks AM, McGlamry RA Neuroarthropathy (Charcot joints) in diabetes mellitus // Journal of American Podiatry Medical Association. 1989. V. 79. P. 110.
8. Stevens M., Edmonds M., Foster A., ​​Watkins P. Selective neuropathy and preserved vascular responses in the diabetic Charcot foot // Diabetologia. 1992. V. 35. P. 148-154.
9. Petrova N., Foster A., ​​Bates M. et al. Can Charcot osteoarthropathy be prevented? // Materials of the annual meeting of the EASD Diabetic Foot Study Group (7-9 Sept. 2001). P.A25.

Key points in the diagnosis and treatment of PDA

• Disturbances of the main blood flow in the lower extremities and diabetic osteoarthropathy are mutually exclusive diseases
• In all cases of unilateral foot swelling in a patient with diabetes mellitus, a PDA should be excluded
• Only timely and “aggressive” treatment can stop the process of destruction of the foot skeleton
• The basis of treatment for PDA is complete unloading of the limb.
• A common mistake is amputation of a foot affected by osteoarthropathy, mistaken for a purulent-destructive process.
• The use of vasoactive drugs worsens the prognosis of PDA
• For patients with diabetic osteoarthropathy, wearing custom-made orthopedic shoes is mandatory

Surgery

Approaches to surgical treatment of DOAP are based on expert opinion and the results of small retrospective studies, in which the majority of reconstructive operations for DOAP were performed by creating arthrodesis according to standard approaches to internal fixation. And to date, there is no convincing data indicating the benefits of one or another form of bone fixation (internal, external or combined) in patients with DOAP of the foot or ankle. An undoubted condition for the use of these methods is the complete subsidence of the inflammatory process and osteolysis, since otherwise surgical intervention may contribute to the emergence of new foci of destruction.

Generally accepted recommendations for surgical treatment of DOAP are:

• surgical intervention is necessary in case of violation of the supporting function of the foot, which cannot be corrected with the help of orthopedic devices and shoes (exostoses, deformities);
• the primary treatment strategy for a fracture with DOAP should not differ from approaches to fractures of other etiologies;
• lengthening the Achilles tendon or gastrocnemius tendon reduces excess plantar pressure on the foot, aligns the ankles and foot in the anterior and middle sections;
• arthrodesis may be useful, despite incomplete consolidation of bone fragments, in patients with instability in the foot, pain and recurrent ulcers during conservative treatment;
• For severe forms of DOAP involving the ankle joint, surgery may be considered as the primary treatment [32].

After surgery, the patient is recommended to be immobilized for up to 7-8 months with dynamic x-ray control and resolve the issue of loading the foot without immobilization. Subsequently, patients often require the manufacture of individual orthopedic shoes.

Neuropathy

Neuropathy - damage to sensory nerves occurs in 70% of patients with diabetes. Nerves in the legs are particularly susceptible to damage because poor diet and high sugar levels destroy the myelin sheath. In the neuropathic form, where a diabetic patient loses sensation in the legs, any microtrauma may go unnoticed until serious ulcers develop.

Signs of foot neuropathy:

• Numbness of the skin
• Tingling
• Pain or burning of the skin of the legs (some forms of neuropathy may cause pain)