Aseptic necrosis of the femoral head is a chronic disease caused by insufficient blood supply to the femoral bones, followed by necrosis and destruction of mineral and cartilaginous tissues, and bone marrow degeneration. The pathology develops after an injury, against the background of concomitant autoimmune diseases, taking hormonal drugs and vascular atherosclerosis.

ANFH is accompanied by acute pain and limited mobility in the hip joint. Dystrophic changes in the structures of the musculoskeletal system lead to a deterioration in a person’s quality of life and severe disability.

ICD-10 code

According to the international classification, aseptic necrosis of the femoral head is designated:

• idiopathic aseptic osteonecrosis of bone – M87.0;
• drug-induced osteonecrosis – M87.1;
• post-traumatic osteonecrosis – M87.2;
• other secondary osteonecrosis of bone – M87.3;
• osteonecrosis, unspecified – M87.9.

Pathogenesis

There are 2 main theories of the development of the disease: traumatic and vascular.

In the first case, pathological processes occur after mechanical trauma, surgical intervention in the femur area, which caused circulatory disturbance in the arteries supplying the subchondral part of the articular surface.

According to the vascular theory, aseptic necrosis of the head of the hip joint develops with atherosclerosis, thromboembolism, vasospasm and other diseases of the arteries supplying blood to the damaged area. Due to circulatory failure, mineral metabolism slows down, weakened structures are easily damaged, microfractures of the tubercles can cause compression of the veins, the formation of blood clots, and impede blood circulation.

The bone does not receive the necessary nutrients, decay products accumulate in the tissues, intraosseous pressure increases, ischemia and necrosis develop. Dystrophic changes are observed in the place of greatest load on the femoral head, the acetabulum suffers to a lesser extent.

Foci of osteonecrosis form 3–5 days after the onset of oxygen starvation, and the dead cells are gradually replaced by osteogenic tissues.

When blood flow is restored, the bone is transformed back to its normal state. But if the head of the hip bone experiences increased load during this period, a zone of perifocal sclerosis is formed. Detachment of articular cartilage occurs, subchondral plates are injured, and cyst-like restructuring of synovial tissues is observed. Destruction is accompanied by the development of reactive arthritis, deforming coxarthrosis, shortening of the femoral neck, and changes in the structure of the acetabulum.

Main causes

ANFH is most often diagnosed in men 30-50 years old; the disease can develop in adolescence. About 50% of patients suffer from bilateral joint damage: the pathological process usually begins with one limb, the second experiences increased stress, and synovial structures undergo similar destruction.

Vascular causes

Why does osteonecrosis of the femoral head develop?

• coronary heart disease;
• atherosclerosis;
• fat embolism of blood vessels;
• decompression when diving to depth for divers and miners;
• sickle cell anemia;
• arterial hypertension.

In the early stages of the disease, the rheological properties and composition of the blood change, vascular spasm develops, and microcirculation is disrupted. A focus of necrosis forms, bone strength decreases, the cartilage tissue of the joint loses its elasticity, which increases the likelihood of deformation of the femoral head.

With atherosclerosis, hypercholesterolemia, and lipid metabolism disorders, fatty plaques form on the walls of blood vessels, which cause arterial obliteration and thromboembolism.

Mechanical reasons

Aseptic necrosis of the hip joint can be caused by the following factors:

• injuries: dislocations, hip fractures;
• consequences of surgical operations in the joint area.

The death of articular tissues occurs several months after injury, but characteristic clinical manifestations appear in patients after 1.5–2 years. The reason may be previous surgical treatment, osteosynthesis, or the use of screws for femoral neck fractures.

Metabolic disorders and pathological conditions

Autoimmune joint damage is accompanied by acute inflammatory processes, the formation of specific antibodies in the blood, which are deposited in the basal layer of the femoral vessels. This leads to poor blood circulation in the bone formations and tissues of the acetabulum.

Non-traumatic causes of avascular necrosis include:

• metabolic disorders;
• autoimmune diseases: scleroderma, systemic lupus erythematosus, vasculitis, rheumatoid arthritis;
• chronic alcohol intoxication;
• osteoporosis;
• pancreatitis;
• osteopenia;
• congenital hip dysplasia.

Patients who take glucocorticoids, cytostatics, and antibacterial agents for a long time are also at risk. Hormonal drugs in high doses cause vasoconstriction and poor circulation in the area of ​​the femoral head.

In 30% of cases, it is not possible to find out the cause of the pathology (idiopathic osteonecrosis of the femur); there may be several provoking factors, which significantly aggravates the course of the disease.

Types and stages of ANGBC

Aseptic necrosis of the femoral heads has 4 stages of development:

1. At the initial stage, the disease is asymptomatic; x-rays do not reveal changes in bone tissue. Stage I is characterized by the appearance of signs of necrosis of the spongy substance of the femoral head, the cartilage remains unchanged. In some patients, mobility in the joint is limited and atrophy of the thigh muscles develops. The stage lasts about six months.
2. Later, sclerotic and destructive changes appear, an impression fracture occurs, and multiple cracks are visible on the surface bone structures. Patients complain of discomfort in the hip area when performing movements.
3. At this stage, a person is bothered by constant pain that occurs after physical activity and does not go away for a long time at rest. Subtotal damage to the head occurs, it thickens, consists of isolated, shapeless fragments, and several foci of compaction or cystic transformation are formed. The joint gap increases, the neck of the femur becomes shorter and thicker. The affected area occupies 30–60%.
4. At stage 4, a dislocation or subluxation forms, the joint is completely devoid of mobility. A person is experiencing intense pain. The head is practically destroyed by 80%, the structure of the tubercles is compacted or dissolved, and has multiple cracks of irregular shape. The necrotic fragment is separated from the bone, may disintegrate into small fragments or dissolve, followed by replacement with connective tissue. The edges of the acetabulum are displaced, the joint space is very small or completely absent. Contractures and hypotrophy of the gluteal muscles are observed.

With the development of deforming arthrosis of the hip joint in adults, secondary changes occur. The head takes on a mushroom shape, increases in diameter, and the cavity flattens.

The examination reveals bone growths (osteophytes), subchondral sclerosis and dystrophic cysts. The process may end with the formation of fibrous ankylosis.

Depending on the localization of pathological changes, ANFH is divided into peripheral, central, segmental and complete. The peripheral type is characterized by damage to the outer part of the femoral head under the articular cartilage. The central focus of osteonecrosis is formed directly in the middle of the head, the segmental one has a cone shape and is localized in the upper outer part.

Symptoms of the disease

Symptoms of aseptic necrosis and ischemia of the femoral head appear gradually. Initially, patients note discomfort and minor pain in the hip joint. The pain radiates to the lumbar region, buttocks, legs, groin, but most often radiates to the knee on the affected side.

Unpleasant sensations in the first stage of the pathology are disturbing both at rest (including at night), and after long walking, being in an upright position, doing physical work, or in bad weather. As the disease progresses, the pain in the joint intensifies and is constantly present, especially when abducting the limb or while getting out of bed. Atrophy of the muscles of the thigh and legs develops, and on one side of the body the buttocks become flattened.

With avascular necrosis, there are no symptoms of general malaise. Due to pain, a person cannot lean on the affected leg, and as a result lameness develops. In the last stages of the death of the femur, you can notice that one limb has become shorter and significantly smaller in volume than the healthy one (by 5–8 cm). A person moves only with the help of support.

Diagnostic methods

Difficulties in making a diagnosis in the early stages arise due to unclear localization of pain and the absence of changes on the x-ray. For this reason, if discomfort occurs in the hip joint, a CT scan is recommended. It is very rare that the presence of symptoms of avascular necrosis is correctly determined; patients are often treated for sciatica, radiculitis, or lumbar osteochondrosis.

Hardware diagnostic methods

Three-phase scintigraphy is used to identify foci of necrosis of the hip joint, its symptoms and prescribe treatment. The patient is injected intravenously with a special marker substance that accumulates in the affected cells. After this, a scan of the joint is performed; if increased radioactive radiation is noted, the development of the pathological process is confirmed.

Radiography

To assess the condition of the bones, an X-ray of the hip joints is performed in 2 study projections. At stage 1, no changes are noted; starting from the second stage, impression fractures, lack of structural pattern, narrowing of the joint space, cystic formations, flattening of the head and shortening of the femoral neck are detected. Most often, radiography is used in combination with other hardware diagnostic methods.

Computed tomography

The most effective way to examine patients with ANFH is computed tomography (CT). Based on its results, the anatomical location and density of bone structures are assessed, and the location of the lesion is accurately determined. CT helps to establish the stage and form of the disease, and to detect signs of bone marrow inflammation in the early stages of the development of aseptic necrosis.

Magnetic resonance imaging

An MRI of the hip joints allows an accurate diagnosis to be made at stage 1 of the disease. The photographs clearly show the inflammatory process in the medulla, primary changes in dense structures, and accumulation of synovial fluid.

The sensitivity of the study is 95–100%.

Tomography makes it possible to accurately determine the stage of the disease, assess the condition of bones and cartilage tissue, and the extent of necrotic changes.

Laboratory research

An analysis of the level of minerals in the blood is prescribed to identify signs of a pathological process and assess the condition of bone structures. With avascular necrosis of the femoral head, the concentration of calcium, phosphorus, and magnesium decreases or remains within normal limits.

Blood composition analysis

A general blood test is not informative.

It is important to determine the ratio of high and low density lipoproteins, the level of creatinine, glucose, and vitamin D.

For autoimmune pathologies, rheumatic tests are prescribed. Immunogenetic and immunoserological studies are necessary to identify genetic diseases, systemic lupus erythematosus. They also conduct studies on the level of thyroid hormones.

Biochemical indicators

With the development of necrosis, not only bones are destroyed, but also protein, which provides strength and elasticity to tissues. During the breakdown of collagen, deoxypyridonoline (DPID) and pyridinoline are formed.

These metabolites enter the systemic circulation and are excreted from the body in the urine. In patients with ANFH, the concentration of protein substances is several times higher than the permissible norm.

Treatment of aseptic necrosis

The method of therapy is selected taking into account the stage of the pathology, the degree of destructive changes, clinical manifestations and the presence of complications. The disease can be treated conservatively and surgically.

Drug therapy

First of all, the attending physician prescribes drugs (Dipyridamole) that reduce ischemia of the femoral head, normalize blood circulation, and eliminate thrombosis. The use of calcium metabolism regulators over a long course of up to 8 months is indicated. Chondroprotectors in combination with vitamins B and D are necessary for the restoration of joint tissues.

Patients must follow an orthopedic regimen, limit the load on the affected limb, and move with the help of crutches. Leg immobilization and daily traction are performed. This allows you to start regeneration processes and prevent damage to the symmetrical joint.

To reduce pain, nonsteroidal anti-inflammatory drugs (Ibuprofen, Celecoxib, Nise) and muscle relaxants that relieve muscle spasms (Mydocalm) are prescribed.

For aseptic necrosis of the femoral head, drug treatment is effective only in the initial stages. Medicines are selected individually for each patient.

Physiotherapeutic treatment

To improve the condition of bone tissue and speed up the recovery process, a course of physiotherapeutic procedures is prescribed. For patients suffering from ANGBS, it is useful to perform electromyostimulation, electrophoresis, UHF, hyperbaric oxygen therapy, laser therapy, take herbal baths, and do acupuncture.

Intra-articular injections

To carry out gas exchange in necrotic areas, injections of a mixture of Perftoran and Dimexide are given into the joint cavity under ultrasound control. Therapeutic manipulations stimulate improvement of blood circulation, oxygen supply in subchondral tissue, regeneration of foci of necrosis, relieve inflammation, and remove toxins. Repeated courses of treatment over a long period of time can significantly slow down the progression of destructive processes and bone necrosis.

Blockades

Novocaine blockades in the area of ​​the lumboiliac muscle help to get rid of severe pain.

After administration of the anesthetic, the conduction of nerve impulses in the lower limb is blocked, and discomfort in the hip joint is reduced.

Hirudotherapy

The use of leeches in the treatment of aseptic osteonecrosis gives good results. By sucking on the skin of the thigh, the leech injects a number of specific enzymes into the patient’s blood. These substances speed up metabolism, resolve blood clots, normalize the functioning of the immune system, and improve blood circulation in the bones.

It is recommended to repeat the course of hirudotherapy 2 times a year. After the first sessions, aggravation and intensification of pain in the joint occurs, relief occurs after 5–6 procedures. This method of therapy is contraindicated for treating children, pregnant women, people suffering from hypotension and hemophilia.

Therapeutic gymnastics and massage

Massage and physical therapy are used as additional treatment methods. During the procedure, the muscles of the back and hips are worked, thereby improving blood flow to problem areas.

Exercise therapy exercises are aimed at strengthening the muscular-ligamentous system, relieving spasms and contractures. The set of classes is selected individually for each patient.

To reduce pain and increase leg mobility, it is necessary to perform dynamic and static exercises that train atrophied muscle groups.

Diet

To lose excess weight, reduce the symptoms of avascular necrosis of the head of the hip joint, and achieve success in treatment, you need to eat right. To strengthen bones, you should add more foods containing unsaturated fatty acids to your diet: sea fish, flaxseed oil. To maintain the elasticity of joint ligaments and cartilage, it is useful to eat lean meats, broccoli, and sweet peppers. Citrus fruits, carrots, pomegranate, and green tea have an antioxidant effect.

Fermented milk products, whole grain cereals, legumes, nuts, pumpkin, and fresh cucumbers help replenish mineral reserves and strengthen bones. If you are overweight, it is recommended to adhere to a low-calorie diet and split meals.

Prohibited foods include fast food, trans fats, processed foods, eggs, and meat by-products. You should not drink coffee or strong tea, and you should completely avoid drinking alcoholic beverages.

Surgery for aseptic necrosis

If conservative therapy does not give the desired results, the disease progresses rapidly and the person cannot lead a normal lifestyle, surgical intervention is recommended. There are several methods of surgical treatment:

• Decompression or tunnelization is the formation of additional holes in the bone structure. This technique allows you to reduce the pressure inside the femur, restore blood flow, and accelerate the germination of new blood vessels. The operation is effective at stages 1 and 2 of ANFH.
• Bone grafting (arthroplasty) is performed by replacing the removed piece of diseased tissue with a piece of musculoskeletal implant taken from the surface of the fibula or artificial calcium sulfate material. The result of therapy is strengthening of the femoral head, elimination of acute pain, and increased blood circulation. The operation can be complicated by thrombosis of the transplanted vessels, and is performed when the disease is of moderate severity.
• Endoprosthesis replacement is the replacement of the affected hip joint with an artificial prosthesis. The patient's head and acetabular socket are completely removed, and a movable structure is installed in their place to perform the functions of a joint. The operation is performed for severe destruction of synovial tissue.

In elderly patients who suffer from diseases that do not allow femoral arthroplasty or endoprosthetics, dead joint tissue is removed and the head and socket are compared for the purpose of fusion.

Unlike other methods, athrodesis is a mutilating operation, after which a person will not be able to walk for about 6 months and becomes disabled.

Rehabilitation

The duration of recovery depends on what treatment was performed. After surgery, rehabilitation is quite long and can last up to 3–4 months. In the postoperative period, the limb is immobilized; the patient must move on crutches and wear orthopedic devices. For bilateral surgery, bed rest is required for 2 months.

To reduce the risk of blood clots, patients are prescribed blood thinning medications. Under the supervision of an instructor, therapeutic exercises are performed to develop the joint, and physiotherapeutic procedures are prescribed. In most cases, by the end of 4 months of rehabilitation, a person begins to move independently without relying on a cane or crutches.

The effectiveness of treatment can be judged by the disappearance of pain. Every 3 months it is necessary to take a control x-ray, take a biochemical blood and urine test, and carry out preventive therapy.

Disability and prognosis for recovery

It is impossible to achieve complete restoration of the joint, but with timely treatment it is possible to slow down the progression of destructive processes in the femur, stabilize the condition, maintain limb mobility and prevent the development of disability.

Description:

The bones of our skeleton consist of bone tissue, which, like most other tissues of the body, consists of living cells and contains blood vessels (arteries, capillaries and veins). If the local blood supply is disrupted, necrosis (necrosis) of a tissue or organ may develop, which can lead to serious problems. Impaired blood supply occurs when there is blockage (thrombosis or) of the arteries that supply blood to a given area. Particularly often, tissue occurs in areas that are supplied with blood from a single artery. Such “problem” areas include the head of the femur. When the blood supply to this area is disrupted, a disease occurs called aseptic necrosis (AN) of the femoral head.

Anatomical aspects:

The hip joint is the largest ball-and-socket joint in our body. It is formed from the deep glenoid cavity of the pelvic bone (acetabular cavity) and the head of the femur. The hip joint is surrounded by powerful muscles (gluteal and anterior thigh muscles). The acetabular cavity and the head of the femur are covered with articular (hyaline) cartilage. Articular cartilage has a very smooth, slippery surface, and its thickness in the hip joint reaches 0.5-0.6 cm. The function of articular cartilage is to reduce friction during movements in the joint and absorb shock loads. The head of the femur is supplied by a single artery that passes through the neck of the femur. Due to the lack of collateral circulation, when blood flow through this artery stops, the blood supply to the femoral head is disrupted. As a result, necrosis (death) of the femoral head develops. Necrosis leads to deterioration of the mechanical properties of bone tissue. Bone is not a “frozen” structure. In bone tissue, bone beams are constantly destroyed and regenerative processes occur at the same time. The cessation of recovery processes due to lack of oxygen and nutrients leads to a rapid deterioration of the mechanical properties of bone tissue. As a result, under the influence of mechanical loads, the necrotic area of ​​the bone collapses (collapses). With the development of AN, the shape of the femoral head changes: it flattens in the area of ​​maximum gravity. As a result, the congruence (articulation) of the articular surfaces in the hip joint is disrupted, which leads to an increase in the internal load during operation of the joint and rapid wear of the articular cartilage. The outcome of AN is the development of osteoarthritis, a degenerative joint disease accompanied by pain and dysfunction.

Causes of aseptic necrosis of the femoral head:

Many factors can lead to the development of AN of the femoral head. Almost any reason that contributes to impaired blood flow in the artery of the femoral head can be an impetus for the development of AN. Thus, traumatic injuries to the hip joint can lead to disruption of the blood supply to the femoral head as a result of mechanical damage or artery damage. The most common injuries leading to the development of AN are hip dislocation. AN develops within a few months, although the first clinical symptoms, as a rule, appear in patients much later (often 1.5-2 years after the injury).
Taking certain medications can also contribute to the development of AN. Most often, AN develops against the background of long-term use of high doses of glucocorticoid hormones for severe, etc. It has been shown that treatment with short courses of hormonal drugs does not increase the risk of developing AN of the femoral head. In this regard, one- or two-time intra-articular or periarticular administration of hormonal drugs in the treatment of osteoarthritis, bursitis, tendonitis and other inflammatory diseases of the musculoskeletal system is also safe. A clear relationship has been observed between excessive alcohol intake and the incidence of AN. Alcohol causes damage to blood vessels, which can cause ischemia of the femoral head and the development of its necrosis. An increased incidence of AN is observed in individuals whose professional activities involve exposure to high pressure (divers, miners). If the decompression regimen is incorrect, small air bubbles form in the blood, which can clog and damage blood vessels, including leading to disruption of blood flow through the artery of the femoral head.

Symptoms of aseptic necrosis of the femoral head:

The first symptom of AN is pain in the hip joint, which occurs when transferring body weight to the “sick” leg. The pain can spread to the groin, buttock area, and radiate (give) along the front surface of the thigh. As the disease progresses, lameness and impaired function (mobility) of the joint appear. In later stages, pain may persist even at rest and contribute to sleep disturbance.

Diagnostics:

Diagnosis of AN begins with a study of the patient's complaints, medical history and physical examination. The doctor will ask you about the presence of chronic diseases, taking medications, and occupational hazards. A question about alcohol abuse may be asked. Physical examination includes examination, palpation of the joint and study of its function (angle of abduction, flexion of the limb, etc.). To clarify and confirm the diagnosis, additional laboratory and instrumental examination methods are necessary.

On radiographs, the AN zone of the femoral head is determined, as a rule, when the disease has had a sufficient duration. In the early stages of the disease, X-ray examination may not detect pathological changes in the bone, despite the fact that the patient may already be experiencing severe pain in the joint. In the later stages of AN, osteoarthritis is added, and it can be difficult to determine which of these diseases is most responsible for the patient’s symptoms.

Radioisotope scanning (scintigraphy)
If there are no pathological changes on radiographs, the doctor may prescribe a radioisotope scan to clarify the diagnosis. With this technique, a medicine containing a radioactive element (radiopharmaceutical) is injected into the patient's body. After a few hours, a special gamma camera is used to record radioactivity in the human body. Due to the lack of blood flow in the head of the femur, this zone on the scintigram (image obtained during scintigraphy) is presented as a “cold” spot, since there is no accumulation of radiopharmaceuticals in it. After the advent of magnetic resonance imaging in clinical practice, the frequency of radioisotope scanning for the diagnosis of AN has decreased significantly.

Magnetic resonance imaging
Currently, magnetic resonance imaging is the most commonly used research method for diagnosing AN of the femoral head. The principle of magnetic resonance imaging is to obtain images of tissues and organs of the body in the form of a series of sections using electromagnetic waves. This is the most informative and completely safe research method. Magnetic resonance imaging can reveal even minor areas with a lack of blood flow in the very early stages of the disease.

Treatment of aseptic necrosis of the femoral head:

Treatment tactics for AN are determined by the stage of the disease and the severity of clinical symptoms. Currently, the effectiveness of drugs aimed at restoring blood circulation in the artery of the femoral head has not been proven. As long as pain can be effectively controlled with analgesic and anti-inflammatory drugs, surgical treatment is usually not required. Although in some cases, if the femoral head has not occurred, the surgeon may suggest surgery to increase the blood supply to the femoral head. There are several options for such operations.

Femoral head decompression
The principle of this simple operation is to drill one or more channels through the neck into the head of the femur, directly into the area where there is no blood flow. This operation has two goals: 1) to increase blood supply to the ischemic area due to the growth of new blood vessels within the drilled channel 2) to reduce intraosseous pressure inside the femoral head and thereby help reduce pain in patients with AN.

This operation is performed through a very small incision on the side of the thigh under the control of an electron-optical converter (EOC). The image intensifier is a mobile digital X-ray device that allows you to obtain images of bones on a display screen directly during surgery. After decompression of the femoral head, the patient must use crutches for 6 weeks. This recommendation is based on the fact that reaming of the canals leads to a temporary decrease in the mechanical strength of the femoral neck, which increases the risk of fracture.

Fibula autograft transplantation
This is a more complex operation that is aimed at increasing blood flow in the ischemic head of the femur. Its principle is to transplant a piece of fibula on a vascular pedicle to the area of ​​the head and neck of the femur. As a result, the ischemic head of the femur receives additional blood supply from the vessels of the bone graft. In addition, the graft mechanically strengthens the femoral head, preventing its further collapse. This operation is performed quite rarely due to its high complexity. The positive effect of the operation is not observed in all patients due to thrombosis of the vessels feeding the bone graft.

Hip replacement
In the later stages of aseptic necrosis, patients develop degenerative joint damage - osteoarthritis. In these cases, hip replacement surgery is indicated to reduce and improve joint function.

As far as I know, this disease is a second group disability. And here the disease is described in detail
www rusmedserv.com

In order for you to be recognized as disabled, you need documentary confirmation from the specialists of the medical institution who make this decision and issue a certificate, and also recommend an individual rehabilitation program for the patient.
Such a certificate is issued after a medical and social examination carried out by a special commission at the institution at the place of residence or place of attachment of the patient. The basis for its holding is a written application from the patient or his legal representative, along with which it is necessary to submit medical documents confirming the violation of his health.
A referral for a medical and social examination is issued by a health care institution or social protection authority. It must indicate data on the patient’s health status, the degree of dysfunction of organs and systems, the state of the compensatory capabilities of his body and the results of the rehabilitation measures taken.
If you are denied such a referral, then you can independently contact the bureau of medical and social examination with documents confirming the impairment of body functions and the associated limitation of life activity.
www dislife ru

Comments

Anastasia, the “social protection authority” never issues a referral to ITU! From what sources does this information come? Please provide a link. A “health care institution” can be a CITO, a clinic, commercial medical institutions, a clinic, and even a children’s dairy kitchen!!! Please, Anastasia, edit your answer with specific information!

Vadim Petrovich, Anastasia is right. A citizen is referred for a medical and social examination by an organization that provides medical and preventive care after carrying out the necessary diagnostic, therapeutic and rehabilitation measures if there is data confirming a persistent impairment of body functions caused by diseases, consequences of injuries or defects. The body providing pensions, as well as the social protection body, has the right to refer a citizen who has signs of disability to MSE if he has medical documents confirming a persistent impairment of body functions. Decree of the Government of the Russian Federation of February 20, 2006 N 95 “On the procedure and conditions for recognizing a person as disabled” www rg ru Ch. III. The procedure for referring a citizen for a medical and social examination

Www rg ru - Order of the Ministry of Health and Social Development of the Russian Federation (Ministry of Health and Social Development of Russia) dated December 23, 2009 N 1013n, Moscow "On approval of classifications and criteria used in the implementation of medical and social examination of citizens by federal state institutions of medical and social examination"
Published March 26, 2010
"3. The main types of dysfunctions of the human body include:
violations of static-dynamic functions (motor functions of the head, torso, limbs, statics, coordination of movements)" - the order is quite large, I hope new data will appear on your blog (website)!

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Aseptic necrosis (osteonecrosis, avascular necrosis) of the femoral head is a multifactorial disease consisting of impaired microcirculation and subsequent necrosis of a section of bone tissue located subchondral in the most loaded upper outer segment of the femoral head, leading to its collapse, disruption of the integrity of the hyaline cartilage covering this area and development of secondary deforming arthrosis.

Aseptic necrosis most often affects men aged 25 to 45 years. 50% of patients have bilateral damage to the hip joints, and 15% of them develop aseptic necrosis of another location (femoral condyles, head of the humerus). The disease is characterized by rapid progression and without proper treatment leads to a pronounced impairment of the static-dynamic function of the joint and, as a consequence, to permanent disability.

A number of reasons can lead to local disruption of microcirculation and the development of a zone of bone necrosis, the most common of which are the first three:

1) damage to the vessels supplying the head of the femur during femoral neck fractures or dislocations of the hip joint;

2) embolization of blood vessels with drops of fat, blood clots, nitrogen bubbles (caisson disease), sickle-shaped erythrocytes;

3) thrombosis in coagulopathies (thrombophilia, hypofibrinolysis) or vascular diseases;

4) vascular occlusion due to external compression due to dislocation, joint effusion, increased intraosseous pressure, hypertrophy of bone marrow cells;

5) damage to the vascular wall by cytotoxic agents.

There are idiopathic aseptic necrosis, which develops spontaneously, for no apparent reason, and secondary, which is associated with the following pathological conditions: long-term systemic therapy with glucocorticosteroids, excessive alcohol consumption, systemic lupus erythematosus and other connective tissue diseases, chronic renal failure, organ transplantation, sickle cell disease. cellular anemia and other hemoglobinopathies, coagulopathies, decompression disease, chronic liver diseases, inflammatory bowel diseases, pancreatitis, hyperlipidemia, gout, pregnancy, radiation sickness, atherosclerosis and other vascular diseases, smoking, Cushing's syndrome, allergic reactions and hypersensitivity, sarcoidosis, chemotherapy and intoxication with chemicals, tumors. 65% of patients with aseptic necrosis of the femoral head have a history of glucocorticosteroid therapy or chronic alcoholism, while idiopathic osteonecrosis is detected in only 15-20% of patients. A significant predisposing factor is the individual characteristics of the vascular anatomy, in particular the collateral-poor lateral vessels of the femoral epiphysis supplying the upper outer segment of the head.

The triggering factor of pathogenesis is a sharp decrease or cessation of microcirculation in the segmental area of ​​the epiphysis of the bone, leading to its infarction, i.e., death of bone marrow cells, stroma and osteocytes. A much larger zone of edema appears around the area of ​​necrosis. Reparative processes begin in bone tissue. However, due to discoordination of spasm and vascular paresis, slowing of blood flow, changes in its rheological properties and aggregation of formed elements, a pathological focus of blood circulation occurs, which is accompanied by the discharge of incoming arterial blood into the venous system of the diaphysis. These changes significantly inhibit reparation, making it ineffective, as a result of which new areas are exposed to necrosis and decompensation occurs. Under the influence of mechanical load, microfractures occur in the subchondral bone, leading to a decrease in its strength. Without underlying mechanical support, hyaline cartilage rapidly undergoes progressive, irreversible degeneration. Violation of the surface structure of the femoral head leads to a change in the mechanical load transmitted to the hyaline cartilage of the acetabulum and the development of pathological changes in it. It should be noted that if the zone of osteonecrosis is limited in area and is located in the medial, less loaded part of the femoral head, then it can undergo spontaneous recovery. The time frame for the development of femoral head collapse ranges from several weeks to several years.

The first clinical manifestation is pain, most often localized in the groin area, less often in the hip, knee joint, or lumbosacral spine.

At first, the pain is periodic, disappearing after rest, and then becomes constant, its intensity gradually increases, intensifying with little physical activity. At a later stage of the disease, pain may occur at night. In some patients, the onset of the disease is sudden. The pain is not accompanied by an increase in body temperature or swelling of the soft tissues in the joint area.

Often in the acute period, patients can neither stand nor walk for several days, then, as a rule, relief occurs with the patient returning to normal physical activity. For several months and sometimes years, normal range of motion in the joint may be maintained. First of all, there is a limitation of rotational movements and abduction, then there is a limitation of movements in the sagittal plane, and ultimately a persistent flexion-adduction contracture and functional shortening of the limb are formed. Characterized by progressive hypotrophy of the soft tissues of the thigh, flattening of the gluteal region on the affected side. A rapidly progressive course of osteonecrosis with significant destruction of the head, early development of deforming arthrosis, dysfunction of the joint and loss of professional ability to work most often occurs with bilateral lesions. With a unilateral process, the main symptoms tend to develop more slowly.

Changes in laboratory parameters are nonspecific.

It is mandatory to perform an x-ray of the hip joint in two projections. In the absence of pathological changes, MRI is indicated, which is the most sensitive method for diagnosing avascular necrosis and allows identifying pre-radiological changes in 90% of patients.

An early radiological sign is a change in bone density in certain areas of the femoral head: you can usually see a very delicate line of reduced density under the subchondral layer of the head, which duplicates the contour of the head and resembles an egg shell. Sometimes it is possible to identify focal areas of rarefaction and, along with them, islands or lines of compaction.

After the appearance of an impression fracture (in the subchondral zone, most often in the upper outer segment of the head), a triangular or disc-shaped area of ​​necrosis is indicated on the radiograph and changes in the contours of the head are revealed, and its deformation most often begins on the lateral edge with a slight impression. The focus of necrosis is revealed as a dense shadow surrounded by a light osteolytic zone, followed by a denser zone corresponding to the zone of sclerosis. Subsequently, secondary changes characteristic of deforming arthrosis occur: beak-shaped bone growths, saddle-shaped deformation of the head, cystic formations, narrowing of the joint space.

Differential diagnosis often has to be carried out with coxarthrosis, tuberculous coxitis, and osteochondrosis of the lumbosacral spine.

Non-operative treatment is symptomatic and is indicated when surgical intervention is not possible. It includes long-term (up to 6 months) limitation of axial load on the affected limb, taking NSAIDs, and physiotherapy (alternating electromagnetic field). In case of secondary aseptic necrosis, it is important to eliminate or correct the effect of the main damaging factor.

If the collapse of the femoral head has not yet occurred, then to prevent it, surgical decompression of the osteonecrosis zone is performed by removing 1-2 cylindrical columns of bone 8-10 mm in diameter, followed by replacing this area with bone allo- or autografts, in the latter case, as free , and on the feeding vascular pedicle. To unload the affected area of ​​the head, corrective osteotomies of the proximal femur are also used. With the development of collapse of the femoral head, total hip replacement is indicated (Fig. 1).

Rice. 1.

Traumatology and orthopedics. N. V. Kornilov

In avascular necrosis of the femoral head, the success of interventions that prevent or prevent femoral head collapse and maintain hip function will be a significant advance in the treatment of this disease.

Core decompression with modification of the technique continues to be one of the safest and most commonly used procedures, with evidence of success in the pre-collapse stage of the femoral head. The additional use of bone morphogenic protein and bone marrow stem cells may provide an opportunity to improve the results of nuclear decompression.

Currently, the use of large vascularized cortical grafts, another surgical procedure with a high success rate, is still not common due to technical difficulties in surgery. Likewise, osteotomies are also not common as arthroplasty is becoming more acceptable, so it is used without any major surgery in between.

In this article you will learn how to treat aseptic necrosis of the head of the hip joint, the causes of its occurrence, characteristic symptoms and preventive measures. As well as the features of the course and treatment of the disease in children and pregnant women.

Aseptic necrosis of the head of the hip joint - characteristics of the disease

Aseptic necrosis of the femoral head (AHNF) or idiopathic necrosis is a serious disease of the hip joint, which is accompanied by necrosis of the bone tissue of the femoral head caused by impaired blood supply and metabolic processes in the head of the hip bone.

In the normal state, the head of the femur is secured by ligaments in the natural depression of the pelvic bone. This depression is called the acetabulum, and it is a rounded depression with smooth walls.