Soft tissue rheumatism symptoms and treatment. Symptoms and treatment of soft tissue rheumatism
Rheumatic diseases of the periarticular soft tissues (synonymous with extra-articular)
characterized by pathological changes in various tissues in the immediate vicinity of the joints - tendons and their sheaths, synovial bags, ligaments, fascia, aponeuroses, subcutaneous tissue. There are primary rheumatic diseases - actually diseases of the periarticular tissues of a dystrophic and (less often) inflammatory nature that occur with intact joints or combined with osteoarthritis.
In their origin, the main role is played by, due to professional, household or sports loads, as well as other endocrine-metabolic disorders (, sugar, obesity), neuroreflex and vegetative-vascular influences that worsen the trophism of periarticular tissues (for example, with osteochondrosis of the spine), congenital inferiority of the tendon-ligamentous apparatus (joint hypermobility), . Secondary rheumatic diseases - predominantly inflammatory lesions of the periarticular formations, due to the transition of the pathological process from the side of the altered joints; are often a manifestation of systemic disease (eg, Reiter's syndrome, rheumatoid arthritis, gouty arthritis). The pathological process is localized, as a rule, in the tendons that carry the greatest load, where, as a result of mechanical stress, defects in individual fibrils, foci of necrosis, secondary with subsequent sclerosis, hyalinosis and calcification occur. The initial changes usually occur in the places where the tendons attach to the entheses. The term "" applies to changes of a different nature that occur at the sites of attachment to the bones of not only tendons, but also ligaments, joint capsules, and aponeuroses. The process may be limited or spread to other areas and his vagina (Tendovaginitis), (Bursitis). Primarily or secondarily, they can be affected (), through which the tendons pass, and sometimes the joint itself (), which sharply limits its function. To refer to these changes, which are clinically difficult to distinguish due to the anatomical proximity of the listed tissue formations, the general term "" ("periarthrosis") is used. Dupuytren's contracture- compaction of the palmar aponeurosis, leading to contracture of the fingers (see Dupuytren's contracture). Rheumatic diseases of the periarticular soft tissues of the lower extremities. Periarthritis of the hip joint is caused by damage to the tendons of the middle and small gluteal muscles at the sites of their attachment to the greater trochanter of the femur, as well as synovial bags in this area. The reasons are, physical, static disorders (shortening of the limb, various diseases of the hip joint). Pain in the upper outer thigh occurs when walking, subsides at rest. Palpation reveals local tenderness in the region of the greater trochanter of the femur. When x-rays can be identified in the region of the greater trochanter, as well as areas of calcified tendons. Periarthritis of the knee joint characterized by pain in the area of the inner surface of the knee joint, appearing with movements and subsiding at rest. On palpation on the medial side of the knee joint below the projection of the joint space, limited soreness of the soft tissues is determined, sometimes their slight swelling and. Popliteal cyst(popliteal bursitis, Baker) occurs, as a rule, with various diseases of the knee joint. In the popliteal fossa, a local limited, various-sized swelling of tissues of a rounded shape containing fluid is determined. large sizes can descend along the intermuscular spaces to the back surface of the lower leg, and also break. In the latter case, there is a sharp pain in the calf muscle, pain on palpation and tissue hyperthermia. Calcaneal tendonitis, plantar aponeurosis and bursitis synovial bags in the calcaneus are characterized by local pain and tenderness on palpation. An X-ray examination can detect calcification of the calcaneal tendon, plantar aponeurosis at the attachment sites in the calcaneus, and in the case of a chronic course of inflammatory changes in these structures in Bechterew's disease and other seronegative spondyloarthritis, superficial destruction (erosion) of the calcaneus. Other rheumatic soft tissue diseases. Diffuse zosinophilic (Schulman) systemic fascia, of an inflammatory (autoimmune) nature, characterized by edema, cellular infiltration, a tendency to adhesion of the tissue of the affected fascia with the subcutaneous tissue and underlying muscles, the development of fibrosis. Morphological features are a sharp thickening of the fascia and the presence of a large number of eosinophils in the composition of cellular infiltrates (the latter is not observed in all cases). not clarified. In a number of patients, the disease is preceded by excessive. The onset is usually acute. Patients note swelling and a feeling of stiffness mainly in the proximal parts of one or more limbs, restriction of movements. Dense edema can also extend to. In some places (usually in the area of the shoulders and hips), the skin acquires an orange peel due to its adhesion to the superficially located altered fascia. Muscle weakness is not observed. Transient, increased ESR, hypergamma globulinemia are characteristic. In some cases, the differential is carried out with systemic scleroderma (Scleroderma) and Dermatomyositis om. In contrast, eosinophilic fasciitis is cured completely with corticosteroids, but this requires many months. Fibrositis(fibromyalgia). These terms are more often used to refer to persistent widespread musculoskeletal pain that does not have a clear morphological basis and is possibly associated with impaired pain perception (pain exaggeration syndrome). It is observed mainly in emotionally labile women. As a rule, there are sleep disturbances, weakness in the morning and stiffness, fast. The pains are aggravated in a stressful situation, in cold damp weather. Palpation reveals painful points characteristic of localization, which the patients themselves are not even aware of: in the region of the trapezius muscles, anterior ribs, external epicondyles of the thigh, etc. ESR and other laboratory tests are not changed. Needed, light gymnastics, as well as weak, analgesics at night. Bibliography: Astapenko M.G. and Erelis P.S. Extra-articular diseases of the soft tissues of the musculoskeletal system, M., 1975; Bosnev V. shoulder - arm, . from Bulgarian, Plovdiv, 1978; Nasonova V.A. and Astapenko M.G. Clinical, p. 535, M., 1989; Travell J.G. and Simons D.G. Myofascial pains, t. 1-2, per. from English, M., 1989.
Lens ectopia, movable lenses, as well as anisocoria observed in Marfan syndrome, lack of pupillary response to light, nystagmus, hydrocephalus, brain dysplasia, diabetes insipidus, autonomic disorders, mental disorders are classified as ectodermal malformations, and intestinal hypoplasia or hyperplasia as endodermal malformations . The prognosis of the disease depends on the severity of cardiovascular disorders. It should be added that the development of aortic insufficiency may occur in patients older than 50-80 years. Sometimes subacute bacterial endocarditis develops.
Ehlers-Danlos syndrome (hyperelasticity of the skin, “looseness” of the joints, “Indian gutta-percha man”) is a disease inherited in an autosomal dominant manner, due to a primary defect in collagen synthesis. Four clinical variants of the syndrome are characteristic: 1) vulnerable skin, the formation of keloid scars due to a deficiency or absence of type III collagen; 2) hyperelasticity of the skin in combination with congenital heart disease in the absence of looseness of the joints; 3) hyperelasticity of the skin, looseness of the joints in combination with eye symptoms, scoliosis due to partial autolysis of collagen due to a deficiency of lysine hydroxylase; 4) hyperelasticity of the skin, looseness of the joints, bilateral dislocation of the hip joints as a result of a disturbed process of converting procollagen to collagen due to a decrease in the activity of procollagen peptidase.
The clinical picture of the disease depends on the degree of influence of the genetic defects of the connective tissue described above and, in general terms, can be manifested by certain signs. Patients sometimes find effusion in the knee joints as a result of constant trauma or looseness of the joints. The gait of such patients resembles the gait of patients with dorsal tabes. Habitual subluxations and dislocations of the clavicular-sternum joint, shoulder joints, head of the radius, and patella are described. In patients, as vivid clinical symptoms, abnormal mobility of the fingers in the interphalangeal joints in the dorsal direction, dislocations of the fingers in the metacarpophalangeal joints are observed. Other characteristic clinical signs include spina bifida, kyphoscoliosis, genu recurvatum, arachnodactyly, deformity of teeth, hernias, flat or hollow foot, blue sclera, ectopic lens, calcified hematomas. The skin has a velvety appearance, reminiscent of wet suede, becomes shiny, thinned. Marked hyperpigmentation of the skin in the area of the knee joints, chin, elbow joints.
Attention should be paid to poor healing of skin wounds, excessive bleeding, although these coagulograms do not show abnormalities. On the part of the internal organs, there are emphysema, pneumothorax, congenital heart defects. With age, hyperelasticity of the skin and looseness of the joints decrease.
DISEASES OF SOFT PERIARTICULAR TISSUES
Rheumatic processes in the periarticular tissues are extra-articular diseases of the soft tissues of the musculoskeletal system, often combined under the general name "extra-articular rheumatism". This large group of pathological processes of various origins and clinics includes diseases of both tissues located in close proximity to the joints, i.e. periarticular tissues (muscle tendons, their vaginas, mucous bags, ligaments, fascia and aponeuroses), and tissues located at some distance from the joints (muscles, neurovascular formations, subcutaneous fatty tissue).
The most studied are diseases of the periarticular tissues, which have clearly defined localization and clinical manifestations, while RB of soft tissues does not
Periarticular, differ in less clear clinical symptoms and often indeterminate localization. As a result, in this section we will only touch on diseases of the soft periarticular tissues.
These processes primarily include tendinitis, tendovaginitis, bursitis, tendobursitis, ligamentitis, and also fibrositis.
Diseases of the soft periarticular tissues are very common. When examining 6,000 people, they were identified in 8% of individuals [Astapenko M. G., Eryalis P. S., 1975]. The defeat of the periarticular apparatus occurs more often in women aged 34-54 years, especially in manual workers.
Pathogenesis and pathological anatomy. Diseases of the soft periarticular tissues can be inflammatory or degenerative in nature.
Inflammatory diseases of these tissues are most often secondary and result from the spread of the inflammatory process from the joint in arthritis of various origins. Independent, primary diseases of the periarticular tissues are based on a predominantly degenerative process, very similar to that observed in arthrosis. Since the causes of the degenerative process in the articular and periarticular tissues are identical, the simultaneous development of degenerative changes in these tissues is often observed, i.e. arthrosis is often accompanied by periarthritis, tendovaginitis and other lesions of the periarticular apparatus. However, a degenerative process (with subsequent slight reactive inflammation) in the soft periarticular tissues with completely intact joints can also often occur.
The similarity of the etiology and pathogenesis of degenerative diseases of the joints and periarticular tissues gives rise to some authors to consider arthrosis and primary disease of the periarticular tissues as clinical variants of a single pathological process.
The primary degenerative process of the periarticular apparatus is most often localized in the tendons (constantly bearing a large load). Due to constant tension and microtrauma in poorly vascularized tendon tissue, ruptures of individual fibrils are observed with the formation of foci of necrosis with hyalinization and calcification of collagen fibers. In the future, sclerosis and calcification of these foci occur, and in nearby well-irrigated synovial formations (vagina, tendons, serous bags), as well as in the tendons themselves, signs of reactive inflammation appear, similar to those that are detected in arthrosis.
The processes described above most often develop at the site of attachment of the tendons to the bone, in the so-called tendon insertions. At the same time, an isolated lesion of the tendon (tendinitis) quickly turns into tendobursitis due to the inclusion of a nearby serous sac in the process. At the same time, due to the reaction of the periosteum, tendoperiostitis develops at the site of contact with it of the affected tendon.
Histologically, in the focus of tendon necrosis, depolymerization of glycosaminoglycans (mucopolysaccharides) is observed with the formation of fibrinoid substance, leukocyte and histiocytic reaction around and subsequent sclerosis and calcification. Most often, insertions of short and wide tendons that carry a large load, such as the tendons of the short shoulder rotators, suffer most often.
With reactive browning in the serous sac, hyperemia, edema with rapid accumulation of serous or purulent exudate in the cavity of the sac is observed. The outcome of this process is mostly favorable: foci of necrosis, exudate and calcifications resolve. However, in some cases, there are residual effects in the form of fibrous fusion of the walls of the bags and the tendon sheath, which makes it difficult for the tendon to slide during its contraction and relaxation and leads to functional disorders.
Although the defeat of synovial formations (synovial sheaths, serous bags) is most often combined with damage to the tendons, however, it can also occur in isolation, sometimes spreading to nearby tendons and causing secondary tendinitis. The degenerative process in the tendons is very often combined with a similar lesion of the ligaments, especially in cases where long and thin tendons pass through narrow ligamentous channels (on the hands and feet). The anatomical relationships here are so close that it is sometimes difficult to resolve the issue of the primacy of the lesion of a particular tissue, i.e., primary tendovaginitis or ligamentitis develops. In these cases, both terms (tendovaginitis and ligamentitis) are often used as synonyms.
The defeat of aponeuroses and wide fascia (fibrositis) is characterized by the predominance of fibrosclerotic processes. They can be widespread (eg, involvement of the entire palmar aponeurosis) or focal (formation of fibrous nodules). In the initial phase, a serous fibrous effusion is observed, which is replaced by a pronounced fibroblastic proliferation with the formation of nodules and subsequent fibroscarring changes, sometimes leading to the formation of persistent contractures.
The variety of pathomorphological changes also causes a large polymorphism of the clinical manifestations of diseases of the periarticular tissues. Thus, the following main processes of periarticular tissues are distinguished.
Tendinitis is an isolated degenerative lesion of the tendon (with little secondary inflammation). This is usually the first short phase of the degenerative process in the periarticular tissues.
Tenosynovitis (tenosynovitis) is often the second phase of the pathological process that develops as a result of contact of the affected tendon with well-irrigated synovial tissues.
Ligamentitis is an inflammatory lesion of extra-articular ligaments; most often the ligamentous canal through which the tendon passes in the area of the wrist and ankle joints.
Calcification - the deposition of calcium salts in the foci of necrosis and serous bags.
Burs and t - local inflammation of the serous bag, which develops most often due to contact with the affected tendon (tendobursitis).
Tendon lesions, in addition, are usually classified according to the predominant localization of the pathological process. The combination of damage to the insertion of the tendon and adjacent formations - the periosteum and serous bag - is called periarthritis. This process most often develops in short and wide tendons that carry a large functional load. The defeat of the middle part of the tendon and its sheath (most often it is thin and long tendons) is referred to as tendovaginitis or tenosipsvit. The lesion, localized in the area of the tendon-muscle ligament, is called m and otend and n, etc.
Fasciitis and aponeurositis - diseases of the fascia and aponeuroses - are commonly referred to by the generic term "fibrositis".
The etiology of independent diseases of the periarticular tissues is very similar to the etiology of arthrosis. The main cause of these painful syndromes is professional, domestic or sports microtraumatization, which is explained by the superficial location of the soft periarticular tissues and their high functional load. It has been established that long-term repetitive stereotypical movements lead to the development of a degenerative process in tendons, collagen fibers and ligaments, followed by slight reactive inflammation in nearby well-vascularized formations - vaginas and serous sacs. This is evidenced by the frequent development of periarthritis, tendovaginitis, bursitis in athletes, dancers, painters, violinists,
typists. Severe physical stress and direct trauma can also cause periarthritis and other soft tissue lesions.
Of great importance are neuroreflex and neurotrophic influences, which worsen the trophism and nutrition of soft periarticular tissues, and contribute to the development of a degenerative process in them. The neuroreflex genesis of such diseases as humeroscapular periarthritis in myocardial infarction, neurotrophic shoulder-hand syndrome, shoulder tendonitis in cervical spondylosis is an established fact.
However, the possibility of developing painful syndromes in the soft periarticular tissues in individuals with a normal load on these tissues (not exceeding the physiological one), in which there is no influence of neuroreflex factors, indicates that there are a number of reasons that reduce the resistance of tissues to the usual physiological load. These primarily include endocrine exchange disorders, as indicated by the frequent development of diseases in women in menopause, especially those suffering from obesity, diseases of the liver and biliary tract. This is evidenced by the frequent combination of periarthritis and arthrosis, which have a similar genesis. As with arthrosis, in this process, the significance of the genetic factor, the congenital weakness of the tendon-ligamentous apparatus or its increased reactivity to the action of various factors that worsen the nutrition and trophism of the periarticular tissues cannot be excluded. The specific mechanisms of the influence of these causes on the development of the degenerative process in periarticular tissues have not yet been studied, but their significance is confirmed by practice.
There are a number of provoking factors contributing to the development of this pathology. The effect of cooling and dampness is well known, which is associated with overstimulation of skin receptors and capillary spasm, which disrupts microcirculation in the periarticular tissues, local metabolism and trophism. Clinical experience shows that a provoking factor in the development of periarticular tissue disease in some cases is a focal infection. In most cases, the occurrence of painful syndromes in the periarticular tissues is the result of a combined effect of several pathogenetic factors.
Clinic. With lesions of the tendon apparatus, clinical manifestations - pain and limitation of movements - are observed only after the inclusion in the pathological process of synovial formations - the tendon sheath and serous bags. The primary isolated lesion of the tendon itself usually does not show any clinical symptoms. The clinical manifestations of soft periarticular tissue disease have some features that allow for differential diagnosis with joint diseases, which sometimes presents difficulties due to close topography, and sometimes close contact of articular and extra-articular tissues (for example, insertions of muscle tendons and epiphyseal periosteum). The pain that occurs when the tendons are damaged, firstly, arises or intensifies only with movements associated with the affected tendon, while all other movements, due to the intactness of the joint itself and other tendons, remain free and painless. Secondly, they appear only during active movements, when there is tension in the affected tendon. Passive movements due to the lack of contraction of this tendon are painless.
On palpation of the affected area, non-diffuse soreness or soreness along the joint space is determined;
as it is observed in diseases of the joints, but local pain points corresponding to the places of attachment to the bone of the insertion of the tendon or the anatomical location of the tendon itself. There is a small and fairly well-defined swelling in the area of the affected tendon or sac (as opposed to diffuse in arthritis).
Localization of periarticular tissue lesions is determined by the intensity of their functional load. The tendons of the hands are mainly affected, which is associated with a multitude and variety of functions of the upper limbs, leading to an almost constant tension of these tendons. Degenerative diseases of the joints are localized, on the contrary, most often in the joints of the legs, which are supporting, therefore, bearing a large functional load.
The most common localization of periarthritis on the upper limb is the area of the shoulder, where the short shoulder rotators and tendons of the biceps muscle are constantly subject to a large functional load, and in difficult conditions (the passage of tendons in a narrow space). This causes the frequent occurrence of tsndoperiostitis of the supraspinatus and infraspinatus muscles, subacromial tendobursitis and tenosynovitis of the long head of the biceps muscle.
In the area of the elbow joint, periarthritis occurs less frequently. Tendoperiostitis usually develops in the area of attachment of the extensor tendons and supinator of the forearm to the external condyle of the shoulder (external epicondylitis). Less commonly, tendobursitis of the tendons attached to the medial condyle of the shoulder (internal epicondylitis) and tendinoperiostitis of the biceps tendon attached to the acromion (acromialgia).
Frequent localization of the degenerative process on the upper extremities are long and thin tendons of the wrist and hand, which pass in narrow fibrous canals. A variety of painful syndromes develop - tendovaginitis of the tendons of the muscles that abduct and extend the thumb (de Quervain's disease), tendovaginitis of the ulnar extensor of the hand (ulnar styloiditis), tendovaginitis of the flexors of the fingers (carpal tunnel syndrome), etc. Damage to the palmar aponeurosis with the development of flexion contracture is much less common. fingers.
On the lower extremities, damage to the tendon apparatus and ligaments is much less common. In the area of the hip joint, tendobursitis of the tendons of the gluteal muscles can develop at the place of their attachment to the large tubercle (trochanteritis) and the iliopsoas muscle at the place of its attachment to the small tubercle.
Tendon bursitis of the tendons develops in the knee area, attaching to the inner surface of the knee and to the tuberosity of the tibia.
The foot and ankle region are the site of the most frequent localization of the degenerative process in the tendons, which, like on the hand, pass through narrow ligamentous canals, as well as at the point of attachment of the Achilles tendon to the calcaneal tuber (achillodynia) and at the point of attachment to the heel bone of the plantar muscles and plantar aponeurosis (with the development of calcaneal bursitis).
The listed lesions of tendons, ligaments and aponeuroses, complicated by the reaction of serous bags and tendon sheaths, can be observed both in isolation and
in various combinations.
In 30-40% of patients, radiographs show calcifications along the affected tendon, as well as a periosteal reaction - compaction and small osteophytes at the site of attachment of the tendon to the bone (tendoperiostitis).
clinical forms. Periarthritis. This is a degenerative lesion of the tendons at the site of their attachment to the bone, followed by the development of reactive inflammation in the affected tendon and in nearby serous bags.
By analogy with degenerative diseases of the joints, lesions of tendon insertions and nearby tissues should be called periarthrosis, since they are based on a degenerative process followed by a slight secondary inflammation. However, according to an established tradition, they continue to be called periarthritis.
Shoulder-shoulder periarthritis (PLP) is the most common form and, according to Robecchi A. (1952), accounts for 80% of all "rheumatic" diseases of the shoulder. This is due to the fact that the tendons of the muscles attached in the area of the shoulder joint are constantly in a state of high functional stress (associated with the abduction and rotation of the shoulder), leading to the early development of a degenerative process in them.
PLP occurs mainly in women over 40 years of age and is more often right-sided, which is associated with a greater load and microtraumatization of the right shoulder, but it can also be bilateral.
The movement of the arm in the shoulder is carried out by a complex physiological system, in which, in addition to the "true" shoulder joint, a large role belongs to the so-called second shoulder joint. This joint is formed not by articular surfaces, but by capsular tendon and musculoskeletal formations. Its upper layer is made up of the deltoid muscle and the acromion, which form the acromiodeltoid arch above the head of the shoulder, and the lower layer is the tendons of the short rotators of the shoulder (supraspinatus, infraspinatus, subscapularis and small round muscles), which, woven into the capsule of the "true" shoulder joint and covering the head of the shoulder , form the so-called rotator cuff of the shoulder. The space between the upper and lower layers is filled with loose connective tissue and serous bags - subacromial and subdeltoid, providing free sliding of both muscle-tendon layers when the shoulder moves (Fig. 55).
Pathological anatomy. There is damage to the insertions of the tendons of the short rotators of the shoulder and the long head of the biceps muscle. First of all, the tendon of the supraspinatus muscle, which is located above the others, is involved in the process, which passes in a narrow gap between the humeral process of the scapula and the head of the shoulder. In second place in terms of frequency of lesions
nia is the long head of the biceps muscle. According to E. Codman (1934),
Rice. 55. Schematic representation of the "true" and "second" shoulder joint at rest (A) and during movement (B).
1 - deltoid muscle; 2 - large tubercle of the head of the humerus; 3 - subacromial bag; 4 - acromion; 5 - supraspinatus muscle; 6 - true shoulder joint (other explanations in the text).
in the initial stage is the rupture of collagen fibrils in the insertion of the tendon
and several foci of fibrinoid necrosis appear on its upper surface. Subsequently, destruction and perforation of the vagina develops with the opening of necrotic contents into the subacromial and subdeltoid bags. In severe cases, there may be a total rupture of the tendon. All these changes are accompanied by reactive inflammation (tendinitis, tenosynovitis and tendobursitis). When the biceps tendon is affected, it becomes uneven and thickened. Hyperemia and edema of the synovial membrane of the vagina with compression of the tendon (acute tenosynovitis) and its subsequent necrosis and growth to the intertubercular groove (chronic tenosynovitis) are observed. Sometimes there may be a rupture of the tendon and dislocation of it from the intertubercular groove.
The consequence of this process is focal (sometimes multiple) calcification of the tendon. In some cases, calcifications can resolve, in others, when the tendon is ruptured, they can enter the subacromial and subdeltoid bags, where acute or chronic reactive bursitis develops. With chronic browning, the walls of the bag can stick together, which makes it difficult to move in the shoulder.
Thickening and wrinkling of the capsule of the true shoulder joint may also develop at the point of contact with the tendons of the short rotators of the shoulder (rectractile, fibrous capsulitis), which significantly limits the mobility of the shoulder.
There are also secondary changes in the nearby bone tissue: compaction of the bone surface of the large tubercle of the head of the shoulder, calcification of the subacromial bursa, slight osteophytosis in this area of the acromion.
Etiology. In the development of the onset of the disease, some predisposing factors are important: age over 40 years, cooling, prolonged exposure to dampness, the presence of a number of diseases in the patient - arthrosis, spondylosis, sciatica, neuropsychiatric disorders, congenital malformations of the upper shoulder girdle.
The main etiological factor is macro and microtrauma (sports, professional). PLP can also appear in patients with coronary disease (more often PLP develops during or in the subsiding phase of an angina attack) and myocardial infarction. According to the observations of de Seze (1966), PLP develops in 10!5% of persons who have had myocardial infarction, and sometimes in patients with hemiplegia. The cause of PLP is often cervical spondylosis with the presence of radicular syndrome, which causes a violation of the trophism of the periarticular tissues of the shoulder and contributes to the development of the degenerative process. According to G. Vignon (1979), a combination of these diseases is observed in 80% of patients with PLP. In many cases, PLP starts for no apparent reason.
Pathogenesis. Most often, in the initial stage of PLP, small focal necrosis or partial ruptures of the fibrils of the supraspinatus tendon are observed without any clinical manifestations. With more pronounced changes, reactive inflammation develops first in the tendon itself (isolated tendonitis), then in the subdeltoid and subacromial bags (acute tendobursitis) with swelling of the tendon and bag. Clinically, this is manifested by severe pain and limited shoulder abduction, which further intensifies the reflex spasm of regional muscles. The capsule of the true shoulder joint is also involved in this pathological process, where retractile capsulitis develops.
With a favorable course of the process, all these pathological phenomena can gradually disappear, in other cases, residual effects are observed in the form of chronic adhesive bursitis and chronic fibrous capsulitis with an outcome in adductor rotator contracture of the shoulder with an intact true shoulder joint.
The main clinical forms of PLP (they can also be stages of the disease) are: 1) simple PLP (“simple painful shoulder” in the terminology of foreign authors; 2) acute PLP (acute painful shoulder); 3) chronic ankylosing PLP (blocked shoulder).
Simple scapulohumeral periarthritis is the initial and most common form of PLP. It is based on isolated tendinitis of the tendons of the supraspinatus or infraspinatus muscle (mainly right-sided), less often the long head of the biceps muscle (Fig. 56). Clinical manifestations are moderate pain and a slight limitation of movement in the shoulder. Pain is localized in the anterior-upper part of the shoulder at the point of attachment of the tendon of the short rotators to the greater tubercle. The most characteristic symptom is the occurrence or intensification of pain with a certain movement of the hand - its abduction and rotation. Usually the patient cannot raise his hand up, and when trying to lay his hand behind his back, he cannot bring his fingers closer to the spine. The remaining movements in the shoulder are free and painless. Sometimes pains appear at night, especially when lying on a sore shoulder.
On palpation, painful points are determined on the anterolateral surface of the shoulder (with damage to the supraspinatus and infraspinatus muscles) or far from the bicipital groove (with damage to the long head of the biceps muscle). Dauborn's sign is very characteristic: the appearance of pain when the arm is abducted to 45-90 ° C (at this moment, the damaged tendon of the supraspinatus muscle and the serous sac between the heads of the shoulder and the acromion are compressed) and subsides after further abduction and raising the arm up. When moving back, the same symptoms are repeated. Pain also occurs when the patient tries to make hand movements when the doctor fixes it (the affected tendon is tensed). The defeat of the supraspinatus muscle is accompanied by pain during shoulder abduction, the defeat of the infraspinatus - with external rotation, and the defeat of the subscapularis - with internal rotation of the shoulder. It is also typical that all passive movements in the shoulder (including abduction and rotation of the shoulder) remain painless. The general condition of the patient and all laboratory parameters are normal. No pathological abnormalities were found on radiography. Only with long-term chronic treatment of the disease, the convergence of bone protrusions (acromion of the large tubercle of the head of the shoulder), their slight sclerosis and osteoporosis as a result of friction against each other, is revealed. The outcome may be a complete recovery within a few days or a week, or a recurrence of the process with a transition to a chronic one, but without significant limitation of movement in the shoulder. With an unfavorable course, acute humeroscapular periatritis or a chronic ankylosing form of the disease may develop.
Acute humeroscapular periarthritis (acute painful shoulder). This form of PLP can be independent or a complication of the previous one. It is based on acute tendon bursitis with calcification of the tendons. The migration of calcifications from the tendons of the short rotators of the shoulder into the subdeltoid bursa with the development of an acute inflammatory reaction in the tendon itself and the bursa causes a hyperalgic crisis. Suddenly, more often after physical exertion, diffuse increasing pain in the shoulder appears, radiating to the neck and back of the arm, resistant to analgesics. The pain is worse at night. Hand movements are severely limited. The patient tries to keep his arm in a physiological position - bent and
brought to the body. On palpation, painful points of various localization are found: on the anteroexternal region of the shoulder (attachment of short rotators), on the outer surface (subdeltoid bag), on the anterior surface (tendon of the long head of the biceps brachii muscle). Sometimes in the region of these points, slight hyperemia and swelling with slight fluctuation (effusion into the serous sac), as well as atrophy of the subacute muscle, are noted. Movement in the shoulder is sharply limited, especially abduction and rotation of the shoulder, while forward movement of the arm is more free. The general condition of patients worsens due to severe pain and insomnia caused by them. There may be subfebrile temperature and increased ESR. Radiographs usually show calcifications in the subacromial region, in the supraspinatus tendon, or, less commonly, in the subscapularis tendon (Fig. 57).
An acute attack of PLP lasts several days or weeks, followed by a decrease in pain and restoration of movement. Slow resorption of calcifications may also be observed. In some cases, the outcome of acute LLP is the formation of adductor rotatory contracture of the shoulder.
Chronic ankylosing humeroscapular periarthritis (locked shoulder)
This is the most unfavorable form, which is based on fibrous bursitis and capsulitis. Usually it is the outcome of acute PLP, but it can develop on its own. Initially, dull pains are observed, aggravated by movements in the shoulder, with characteristic localization (painful points at the points of attachment of the tendons) and irradiation. The most characteristic symptom is progressive stiffness of the shoulder. Both the lateral abduction of the shoulder (it is carried out only due to the scapular-sternal articulation, and when the scapula is fixed becomes impossible) and internal rotation are sharply disturbed. The absence of contractions of the adductors (pectoralis major and serratus) when trying to abduct the arm, an increase in the range of motion in the shoulder with local infiltration of anesthetics indicates the mechanical nature of the blockade of the shoulder.
On palpation, pain is determined in front of the acromion, below it, along the groove of the biceps muscle of the head of the shoulder and at the place of attachment of the deltoid muscle to the shoulder. The general condition of patients, body temperature and laboratory parameters are normal. X-rays may show calcifications along the affected tendons.
Much less often, other variants of the disease are observed that occur due to the predominant lesion of the tendons of the subscapular, coracobrachial, long head of the biceps and deltoid muscles.
Insertion of the tendons of the subscapularis and coracobrachialis muscle proceeds with pain and pain points localized in the region of the coracoid process on the anterior surface of the shoulder, while the subacromial region (anterolateral surface of the shoulder) and the region of the biceps sulcus are painless.
External rotation and posterior flexion are most limited, and shoulder abduction, the opposite of the typical form, is only partially limited. No pathology was noted on the radiograph.
Tenosynovitis of the long head of the biceps brachii muscle occurs mainly in men due to tendon injury (a sharp movement in the shoulder or a blow to its front surface). The disease is manifested by spontaneously occurring pain on the anterior surface of the forearm and pain on palpation of the head of the shoulder. Flexion and extension of the arm bent at the elbow is painful, especially if these movements are made by other persons, and the patient resists this movement (Ergazon's test). Pain also appears during external rotation of the lowered arm, produced under the same conditions (with the patient's resistance). These tests are of diagnostic value. The appearance of pain is associated with tension and compression of the damaged tendon of the long head of the biceps muscle in a narrow groove.
Insertionitis of the tendon of the deltoid muscle is rare, mainly with a sports injury ("golf shoulder"), and is manifested by pain and palpation tenderness at the point of attachment of the deltoid muscle to the outer surface of the upper third of the shoulder.
In coronary disease and myocardial infarction, in 10% of cases, PLP can develop (more often left-sided, sometimes even bilateral) due to reflex neurovascular disorders caused by myocardial ischemia, as well as limitation of motor activity of the upper shoulder girdle, which worsens blood circulation in the tendons and contributes to the development of a degenerative process in them. In these cases, PLP occurs either against the background of frequent angina attacks, or 1-6 weeks after myocardial infarction. Clinical manifestations are moderate pain and slight limitation of movement.
in shoulder (especially abduction), which is accompanied by a feeling of coldness of the hand, its increased sweating and cyanotic skin tone. An x-ray showed osteoporosis of the humeral head and acromion. The occurrence of PLP syndrome in these patients is often erroneously interpreted as an exacerbation of coronary artery disease. When conducting differential diagnosis
in the benefits of PLP are evidenced by: the occurrence of pain only with certain movements in the shoulder, the absence of the effect of vasodilators and correlations with other symptoms of myocardial ischemia (for example, with changes in the ECG).
Cervical spondylarthrosis with secondary radicular syndrome can often be combined with PLP, which is explained by neurovasomotor and trophic disorders of the periarticular tissues of the shoulder, resulting from a pathological process in the roots. Concomitant vegetative-vascular signs are characteristic of this variant: edema and cyanosis of the skin of the hand, a feeling of "crawling", etc.
Algodystrophic syndrome "shoulder-hand" was described by V. Steinbroker in 1967, characterized by severe causalgia, pronounced vasomotor-trophic symptoms in the form of diffuse cold dense edema, cyanosis of the hand and fingers, thinning of the skin, brittle nails, atrophy of muscles and subcutaneous adipose tissue, gradual development persistent flexion contracture of the fingers (Fig. 58). Movements in the shoulder and hand are sharply limited. The elbow joint, as a rule, remains intact. The radiograph reveals pronounced patchy osteoporosis, restructuring of the bones of the hand and the epiphysis of the radius. These symptoms belong to the group of neuroreflex algodystrophies that occur due to organic damage to the sympathetic fibers of the peripheral nerves and proceed with severe pain and impaired tissue trophism.
According to V. Wright (1979), the “shoulder-hand” syndrome can be: idiopathic (23%), post-infarction (20%), caused by spondylosis of the cervical spine (20%), post-traumatic (10%), combined (11% ), posthemiplegic (6%) and associated with other causes (10%).
The course of all algodystrophies and, in particular, the “shoulder-hand” syndrome is very long.
trophic disorders. Sometimes a few months after the onset of the disease, a symmetrical shoulder and hand are affected.
In some neurological processes (hemiplegia, parkinsonism, brain tumors), humeroscapular periarthritis may develop, in the genesis of which neuroreflex disorders are of primary importance. Hemoplegia can be observed: 1)
isolated | ||
58. Dense diffuse edema iee and hand with syndro- |
||
"shoulder - brush". | ||
tendinitis with clinical symptoms of a simple disease |
||
sore shoulder; 2) retractile capsulitis with development |
||
"blocked shoulder"; 3) secondary stretch | ||
ki with looseness of the shoulder joint (“falling shoulder |
||
Diagnosis. Diagnosis of humeroscapular periarthritis depends on the form of its course. The simple form is characterized by: 1) pain in the upper part of the shoulder during abduction and rotation of the arm; 2) painful points
on palpation of the anterior outer part of the shoulder or in the area of the intertubercular furrow; 3) limitation of abduction and rotation; 4) signs of Dauborn (in case of damage to rotators), Ergazon (in case of damage to the long head of the biceps muscle of the shoulder); 5) X-ray narrowing of the gap between the acromion and the head of the shoulder, osteosclerosis and osteophytosis of the large tubercle and acromion.
Acute PLP is characterized by: 1) acute diffuse pain in the shoulder with irradiation to the neck and arm; 2) a sharp limitation of movements in the shoulder; 3) sharp soreness and slight swelling of the anterior outer surface of the shoulder; 4) the presence of calcifications in the area of the tendons and radiological intactness of the first shoulder joint.
In chronic PLP, the following are noted: 1) moderate pain of the same localization (mainly when moving with resistance);
2) significant progressive limitation of movement in the shoulder (especially rotation
and leads); 3) symptoms of "mechanical blockade"; 4) osteoporosis of the head of the shoulder, calcifications in the subacromial region, intactness of the shoulder joint on the radiograph; 5) the presence of retractile capsulitis on contrast radiography and arthropneumography.
Differential diagnosis is carried out with arthritis and arthrosis of the shoulder, acromioclavicular joints and cervical spine. It is necessary, however, to remember the possibility of a combination of degenerative lesions of the joints and periarticular tissues.
Periarthritis of the elbow joint. This disease develops due to degenerative changes in the tendons of the elbow at the place of their attachment to the external or internal
epicondyles of the shoulder or to the olecranon (olekration). Usually there is also a reaction of the periosteum, i.e. tendoperiostitis develops. The most commonly affected tendons attach to the lateral condyle of the humerus. In accordance with the localization, the following types of ulnar periarthritis are distinguished.
External epicondylitis of the shoulder (tennis elbow) - tendon injury
batel of the hand and fingers, long supinator of the forearm, characterized by pain in the area of the external epicondyle (outer surface of the elbow) and pain limitation of movements. The disease is associated with a professional or sports injury in individuals who often repeat stereotypical movements in the elbow - extension and supination of the forearm (for example, in masons, carpenters, tennis players, masseurs, painters, people of heavy physical labor).
In men, external epicondylitis is more common and is usually right-sided.
In the pathogenesis of the disease, the tension of the tendon insertions with partial separation of some fibrils from the place of their attachment to the bone is important, as well as the infringement of the tendons by the aponeurosis on the bone protrusion at the time of their contraction, which leads to impaired circulation. The development of epicondylitis is also facilitated by cervicoarthrosis with radicular syndrome, which is often combined with it.
The main symptom of epicondylitis is pain in the external epicondyle, radiating up the outer edge of the shoulder and down to the middle of the forearm. Pain appears only with extension and supination of the forearm, especially with a combination of these movements. Passive reproduction of these movements is painful only when the patient is resisted. The pain intensifies when the hand is clenched into a fist while it is bent at the same time (Thompson's symptom). Palpation of the external epicondyle of the elbow is painful. The strength of the brush is reduced. Radiologically determined periosteal phenomena, slight calcification and ossification of the tendons near the external epicondyle.
The course of the disease is chronic. When resting the affected tendons, recovery may occur in a few weeks or months. However, in some cases, the disease can last for several years, recurring with repeated occupational or sports microtrauma.
Internal epicondylitis of the shoulder, or epitrochleitis, due to degenerative
changes in the tendons of the flexors of the hand, fingers and one of the heads of the round pronator of the forearm. It is rare, develops mainly in people doing light physical work (seamstresses, typists, etc.). The main symptom is pain during flexion and pronation of the forearm, radiating along its inner edge.
Palpation of the internal epicondyle is painful. Passive movements are performed freely. There is no radiological pathology. The course is chronic, but when resting the affected muscles, recovery can occur.
Olecranalgia is characterized by pain in the olecranon region resulting from degenerative changes in the triceps tendon insertions attached to olecranon. The disease can begin for no apparent reason or after an injury. The pain is permanent and aggravated by extension of the forearm and pressure on the olecranon. X-ray revealed a small periosteal reaction (tendoperiostitis).
The course of the disease is chronic and very persistent. The diagnosis is made on the basis of the following symptoms: 1) pain in the area of the external epicondyle during extension and supination of the forearm (epicondylitis), internal epicondyle during flexion and pronation of the forearm (epitrochleitis), olecranon during extension of the forearm (olecranalgia); 2) pain when pressing on the epicondyles of the shoulder and olecranon; small periosteal phenomena in these areas on the radiograph.
Periarthritis of the wrist joint. The most common variant of the disease is radiation styloiditis. It is based on tendoperiostitis of the tendon of the long supinator of the forearm at the site of its attachment to the styloid process of the radius. Mostly women aged 40-60 are ill (most often dressmakers). Styloiditis is usually right-sided, which indicates the importance of frequent microtraumatization.
The pathogenesis of the development of styloiditis is the same as that of epicondylitis - degenerative changes and detachment of some fibrils occur with their constant tension and tension due to the peculiarities of the profession.
The main clinical symptom is pain in the region of the styloid process of the ray (slightly above the inner edge of the wrist joint), which is aggravated by supination of the forearm. There is a slight localized swelling in this area. On palpation, the area of the process is painful. X-ray shows periosteal reaction, cortical thinning, and osteoporosis of the styloid process.
The course of the disease is long and persistent (several months). There is resistance to any treatment.
Periarthritis of the hip joint (trochanteritis). The disease is based on degenerative changes and a secondary inflammatory process in the tendons of the middle or small gluteal muscles at the sites of attachment to the greater trochanter of the femur. Usually, inflammation of nearby serous bags joins, i.e. tendobursitis develops. In most cases, the lesion is unilateral. Women aged 30-60 get sick more often. The main causative factors are trauma and physical overload of the tendon. The development of the disease is favored by hypothermia, a sedentary lifestyle, and obesity. Overloading of the tendons of the gluteal muscles can be the result of static changes (scoliosis, lordosis, kyphosis), as well as atrophy of the quadriceps muscle, asymmetry of the lower extremities. Being in most cases 1.а1уц)Stoyatel'n1|U| disease, trochanteritis sometimes develops with coxarthrosis as a secondary syndrome.
The main clinical symptom is attacks of pain in the area of one of the hip joints. The pain is localized on the outer surface of the buttock in the region of the greater trochanter or inguinal fold and radiates to the thigh. The pains are aggravated by walking, at night and subside in a state of complete rest. The development of an attack is in the nature of a crisis, with rapidly increasing severe pain, causing a significant limitation of all movements in the joint. An objective examination reveals painful points around the greater trochanter with a sharp increase in pain when pressing on its posterior superior angle. At the height of the attack, all movements in the joint are limited, after it subsides, only internal rotation. Pain increases with hip abduction, especially when the patient resists this movement.
In the area of the greater trochanter, slight swelling and hyperemia of the skin may occur. There may be fever and an increase in ESR.
X-ray in 25% of cases, calcifications are found near the greater trochanter (Fig. 59). Sometimes you can see calcification of the tendons of the gluteal muscles (dense strands going up from the upper edge of the greater trochanter, osteophytes in the region of the greater trochanter and along the superior iliac crest).
Trochanteritis can have several clinical variants. The most typical form is calcific periarthritis, which occurs in the form of an acute pain crisis, resembling acute coxitis. The attacks last for several days, then the pain gradually subsides, the movements are restored, but for a long time there are painful points in the region of the greater trochanter and pain during internal rotation of the thigh.
With the development of chronic tendobursitis, the course of the disease is protracted, recurrent. X-ray revealed calcifications in the tendons of the gluteal muscles and serous bags.
Non-calcifying periarthritis occurs more easily in the form of small pain attacks that occur after cooling and physical exertion. At the same time, pain points appear with
Rice. 59. Pe-
arthritis of the hip joint. Calcifications in the greater trochanter.
characteristic localization and pain with extreme movements in the thigh. Radiological pathology is not observed.
In some cases, there is a syndrome of "springing" or "clicking" hip - a short-term sensation of an obstacle at the level of the greater trochanter and the resulting intermittent movement of the hip during flexion and extension. When overcoming this obstacle, a click and slight pain are felt. This is due to thickening and fibrosis of the broad fascia of the thigh, which interferes with the movement of the greater trochanter. The occurrence of this syndrome is favored by the presence of bursitis and exostoses in the region of the trochanter.
The diagnosis of trochanteritis is made on the basis of the patient's complaints of sudden progressive pain in the hip joint, significant movement restrictions, and rapid favorable evolution of the disease.
The disease should be differentiated from osteochondrosis and spondylosis with the presence of radicular syndrome, acute coxitis and coxarthrosis.
Periarthritis of the knee joint is essentially tendinitis or tendobursitis of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendons of the tendon of the tendon of the tendon of the tendon of the semimembranosus and tendons of the tendons of their attachment to the internal lateral ligament (the so-called tendons of the goose foot). The disease occurs as a result of domestic, professional or sports microtraumatization of the knee. Due to frequently repeated flexion and external rotation of the knee joint,
there is a strong tension of the tendons with the development of degenerative processes and secondary inflammatory reactions in them.
The main clinical symptom is persistent pain.
and pain on palpation of the inner surface of the knee joint, which occurs when walking (at the moment of bending the leg at the knee) and during prolonged standing. Local hyperemia and slight swelling are possible.
Flexion, extension and external rotation of the lower leg are painful. X-ray pathology is not detected. At rest and with appropriate treatment, full recovery occurs.
It is necessary to differentiate the disease from the following post-traumatic syndromes: 1) post-traumatic bursitis, also manifested by pain and swelling in the patella; 2) post-traumatic lipoarthritis (Goff's syndrome). characterized by slight pain in the knee on movement and painful swelling on both sides of the patellar ligament; 3) Hooke's periarthritis - fatty infiltration of the periarticular and intraarticular tissue with an increase in the size of the joint, doughy consistency of the periarticular tissues, their compaction on the radiograph, difficulty in moving in the joint; 4) Pellegrini syndrome - Stida - post-traumatic ossification of the periarticular tissues in the area of the inner condyle of the thigh, manifested by pain and the formation of a very dense tumor. X-ray revealed large soft tissue calcifications of the medial surface of the knee. In addition to post-traumatic syndromes, periarthritis of the knee joint must be differentiated from early forms of arthritis and arthrosis of this joint.
Periarthritis of the foot (thalalgia, achillodynia, calcaneal spurs). The common thalalgia syndrome (pain in the heel) occurs due to damage to the Achilles tendon insertions attached to the outside of the calcaneus, insertions of the tendons of the plantar muscles and plantar aponeurosis attached to the plantar side of the calcaneus.
Damage to the tendon apparatus of the foot can be either degenerative (primary) or inflammatory (secondary). Degenerative damage to the Achilles tendon and tendons of the plantar muscles occurs due to their microtraumatization during walking and running, when, with constant strong tension of these tendons with pulling out of some fibrils, foci of degeneration form in them, followed by tendoperiostitis. When the process spreads to nearby serous bags, phenomena of suprachecal and subcalcaneal tendobursitis occur. All these interrelated processes are denoted by the term achillodynia.
The pathological process ends with ossification of the affected tissues with the formation of exostoses at the site of attachment of tendon insertions along the posterior and lower surfaces of the calcaneus - calcaneal spurs, which are often bilateral. The development of reactive inflammation in the tissues surrounding exostoses, as well as the presence of tendobursitis and tendoperiostitis, are clinically manifested by thalalgia.
There is usually no direct correlation between the size of the calcaneus spurs and the intensity of thalalgia. In addition to constant microtraumatization (overloading the foot, wearing narrow shoes), damage to the tendons of the foot can be caused by a single severe injury, vasomotor and trophic disorders in the tissues in the heel area.
Clinic. Characterized by pain in the heel region that occurs when stepping on the heel and when the sole is bent. In the area of attachment of the Achilles tendon, there is a round, painful swelling (Achilles bursitis), and the tendon itself is thickened and painful on palpation (Achilles). Pressing on the heel from the sole causes severe pain due to the presence of subcalcaneal bursitis. There is no pain at rest.
On the radiograph, exostoses (“spurs”) are found on the posterior and (or) plantar surfaces of the calcaneus and periosteal phenomena. Symptomatic (secondary) thalalgias occur most often in systemic non-infectious diseases of the joints - rheumatic and rheumatoid arthritis, ankylosing spondylitis, etc. as one of the manifestations of the general pathological process. In metabolic diseases - gout, xanthomatosis and amyloidosis, thalalgia develops due to infiltration of the Achilles tendon with urates, xanthoma or amyloid masses.
Diagnosis. When diagnosing peri-arthritis of the foot, it is important to take into account the presence of pain during the onset and pressure on the heel, which subsides at rest, Achillitis and Achilles bursitis, calcaneal spurs, detected on the radiograph. Diagnosis of all primary periarthritis is based on the presence of common signs:
1) pain that occurs only with certain movements associated with the participation of the affected tendon; 2) limited, superficial swelling at the site of inversion of the tendon or serous sac; 3) strictly local pain on palpation (pain points); 4) restriction of certain active movements; 5) normal volume of passive movements, the occurrence of pain only when the patient resists these movements; 6) the intactness of the corresponding joint and the presence of signs of periarthritis (on radiographs, small periostitis, osteoporosis and osteophytosis at the site of attachment of the affected tendon, thickening and calcification of the soft periarticular tissues); 7) absence of inflammatory diseases of the joints.
differential diagnosis. The disease is differentiated primarily from inflammatory and degenerative processes in the joints. We present the main differential diagnostic criteria (Table 18).
Treatment. Given the tendency of all primary periarthritis to a persistent and prolonged course, the cause of which is a very slow resorption of foci of degeneration and calcifications,
Table 18. Differential diagnosis of arthritis, arthrosis and periarthritis
Periarthritis | |||||||
Spontaneous | mechanical |
||||||
whether, strengthen- | type for all |
||||||
eat with all | movements |
||||||
Swelling | Malobolez- | Painful | Missing |
||||
limited | diffuse, | ||||||
Sus deformation | Missing | Expressed for |
|||||
jumpy | bone count |
||||||
growing up |
|||||||
Soreness | Local | Missing or |
|||||
diffuse, |
|||||||
palpation | painful | stricken | slightly pronounced |
||||
Skin Boost | Missing | Expressed | Missing |
||||
noah temperature- | more expressed | May be | |||||
Skin hyperemia | Missing | ||||||
smitten | |||||||
Passive motors | limited | In full |
|||||
limb | weakly |
||||||
Active movements | limited | limited | In full |
||||
limb | some | movements | or slightly ogre |
||||
Laboratory | Missing | indicate | |||||
Missing |
|||||||
indicators of active | |||||||
sti inflammatory | body | ||||||
process | Absence | Signs of arthro |
|||||
Radiography | signs |
||||||
cov arthritis and | for: narrowing the sus |
||||||
fiqats and pe- | theoporosis | chondral wasp |
|||||
theosclerosis, os- |
|||||||
as well as the usually ongoing microtraumatization of the tendon, a necessary condition for proper treatment is its duration and persistence. The main methods of treating periarthritis are unloading the affected tendon, the use of painkillers and anti-inflammatory drugs, physical and balneological methods, and sometimes surgical intervention. Immobilization of the diseased limb is used to create rest for the affected tendon. In mild cases, this is achieved by the use of support bandages (wearing a handkerchief), simple wooden or wire splints that limit the mobility of the limb. After several days of such immobilization, recovery may occur. In more severe cases, a removable plaster splint is used. After the pain decreases, cautious light movements begin, first active, and then passive. At the same time, analgesics are used (acetylsalicylic acid, analgin, brufen, indocide, butadion, reopyrin, etc.) in usual doses.
With persistent pain, the affected area is infiltrated with novocaine in combination with hydrocortisone. With PLP, hydrocortisone is injected into the subacromial or subdeltoid region (50-100 mg), with trochanteritis - in the region of the greater trochanter (30-50 mg), with epicondylitis - in the region of the external epicondyle, with styloiditis - in the region of the styloid process of the radius (20 -39 mg), with thalalgia - in the area of attachment of the calcaneal tendon or in the plantar part of the foot (20-30 mg). Injections are repeated after 5-10 days until the pain decreases. With very acute pain, it is possible to use corticosteroids inside (prednisolone or triamcinolone, 2-3 tablets per day, followed by a slow decrease in the dose of 1/4 tablet for 5 days).
GCS quickly reduce pain and exudative phenomena in the tissues, but do not prevent the development of stiffness and therefore are only part of the complex treatment of periarthritis.
Physical methods of treatment (ultrasound, hydrocortisone phonophoresis, sinusoidal currents, etc.) have a good analgesic effect and improve blood circulation. With persistent pain syndrome, X-ray therapy can be used, with a protracted chronic course, general radon and hydrogen sulfide baths are indicated.
The best way to prevent shoulder blockade in chronic PLP is systematic therapeutic exercises, applied for several months. Massage with periarthritis is contraindicated. In mild cases, a light massage of the limb can be applied with a bypass of the affected area and only when the pain subsides.
With the ineffectiveness of all methods of conservative therapy, surgical treatment is used.
The prognosis for periarthritis is usually favorable. Gradually, resorption of foci of degeneration and calcifications occurs, the disappearance of pain and restoration of limb mobility. In protracted and persistent cases, fibrous adhesions of the affected tissues and persistent functional insufficiency are formed.
MYOTENDINITIS
The defeat of the tendon at the point of its transition to the muscle (musculotendinous ligament) is called myotendinitis.
Due to the less traumatization of this part of the tendon, its defeat is much less common than periarthritis, and occurs only with a significant and prolonged overload of the tendon - in soldiers during military exercises, in athletes during intensive training, in workers of hard physical labor. Most often, the extensor of the hand and foot is affected (general extensor of the fingers, extensor of the thumb, Achilles tendon, etc.).
Clinic. Typical signs: pain during movements involving the affected tendon and painful points localized at the beginning of the tendon. For example, with damage to the radial extensor of the hand, pain, slight swelling and hyperemia of the skin are localized on the back of the hand, with damage to the muscles of the thumb - on the forearm slightly above the styloid process, with damage to the Achilles tendon - above the heel. For the defeat of the tendons of the muscles of the thumb of the hand, the appearance of a painful swelling in the lower third of the forearm is characteristic, palpation of which during the movements of the thumb crepitus is felt. With active movements involving the affected tendons, severe pain occurs, while passive movements remain free and painless. No pathology was found on the radiograph.
The course is long, persistent (up to several months). With the transition to ordinary work, the disease may recur. At rest and with appropriate treatment, recovery occurs.
Treatment. First of all, it is necessary to create rest for the affected tendons, which is achieved by immobilizing the limb in a plaster splint. To reduce the pain syndrome, various analgesics are prescribed, with severe persistent pain, the affected area is infiltrated with hydrocortisone or X-ray therapy.
TENDOVAGINITIS (TENOSYNOVITIS) AND LIGAMENTITIS
Tenosynovitis is a degenerative or inflammatory lesion of the middle part of the tendons, mainly those that are clad in tendon sheaths and pass through narrow ligamentous canals. This takes place in the wrist and ankle regions. Usually, all closely adjacent tissues are affected - the tendon, its synovial sheath and ligamentous canal. Therefore, the terms "tendovaginitis", "tenosynovitis", "ligamentitis" are often used as synonyms, especially since it is sometimes impossible to determine the location of the primary lesion. Difficulty sliding the tendon along the ligamentous canal may be due to nodular thickening of the tendon itself, proliferation and thickening of the synovial sheath, or cicatricial narrowing of the ligamentous canal. It is known that the dorsal ligament of the wrist has 6 ligamentous canals. The defeat of the I channel, through which the tendon of the short extensor and adductor of the thumb passes, leads to the occurrence of stenosing tendovaginitis of these tendons (de Quervain's disease); with damage to the VI channel, through which the tendon of the ulnar extensor of the hand passes, stenosing tendovaginitis or ligamentitis of this channel develops (synonymous with ulnar styloiditis).
On the palmar surface of the hand is the palmar ligament of the wrist, under which there is a ligamentous canal. With the development of a pathological process in the synovial sheath of the flexors of the fingers (passing through this channel), these sheaths are compressed, as well as the branch of the median nerve located here, which is clinically manifested by symptoms referred to as “carpal tunnel syndrome”. In the palmar ligament of the wrist there is a so-called Guyon canal through which the ulnar nerve and ulnar artery pass. With the defeat of this canal and the compression of the formations passing through here, the so-called Guyon canal syndrome develops. Similarly, tendovaginitis and ligamentitis of seven channels develop, located on the back of the foot in the ankle region, as well as on the plantar surface of the foot and its heel part.
There are three forms of the pathological process in tendovaginitis: 1) mild, or initial form, in which only hyperemia of the synovial sheath with perivascular infiltrates in its outer layer is observed, a similar picture is observed mainly when the tendon of the extensor and flexor tendons of the hand, feet and fingers is damaged; 2) exudative-serous form, characterized by the accumulation of a moderate amount of effusion in the synovial vagina, and clinically manifested by a small round swelling in this area;
a similar picture develops with carpal or Guyon canal syndromes, and with tendovaginitis of the peroneal muscles;
3) chronic stenosing form with sclerotic changes in the synovial sheaths, erasure of the structure between the individual layers and stenosis of the vagina; a manifestation of this form is, for example, de Quervain's stenosing tendovaginitis, "trigger finger", etc.
Tendovaginitis can be secondary, accompanying various diseases of the joints, infectious or allergic processes, or primary, independent. The causes of primary tendovaginitis of the wrist region are most often professional or sports microtraumas, tendovaginitis of the ankle region - static anomalies (flat feet, clubfoot, genu varum et valgum), prolonged standing, sports micro and macrotraumas, varicose veins, thrombophlebitis, lymphostasis.
In the clinical picture of tendovaginitis, the main symptoms are pain during movement involving the affected tendon, local tenderness and swelling of the tendon. In some cases, atrophy of the corresponding muscle is observed.
X-rays sometimes show soft tissue thickening in the area of the affected tendon. Laboratory parameters are normal. Sometimes, in acute forms, ESR can be somewhat accelerated.
The main clinical forms of tendovaginitis. De Quervain's disease. At the heart of
The disease is tendovaginitis of the short extensor and long abductor of the thumb or stenosing ligamentitis of the I canal of the dorsal carpal ligament. The narrowing of the I channel leads to compression of the tendons and their sheaths, which is manifested by pain in the region of the styloid process of the radius. The causes of the development of the disease are trauma or prolonged microtrauma of the corresponding tendons.
De Quervain's disease is the most common form of all stenosing tendovaginitis of the wrist region (95% of all tendovaginitis), which is explained by the greatest overload of the thumb during hand movements. People with heavy physical labor (miners, loaders, masons, metalworkers, etc.), as well as people whose work is associated with constant muscle tension in this area (seamstresses, pianists, etc.) get sick.
Clinic. Spontaneous pains are characteristic, aggravated by extension and abduction of the finger in the region of the styloid process of the radius, radiating to the first finger or towards the elbow, as well as a decrease in the strength of the first finger. In the region of the styloid process of the ray, severe pain, clearly limited, inactive swelling is determined. The pain sharply increases with the patient's resistance to the doctor's effort to bring the abducted thumb (a positive test for tense abduction of the thumb). Elkin's test is also positive - sharply painful reduction of the tips of the thumb and IV and V fingers of the hand.
Laboratory indicators of the inflammatory process (ESR, leukocyte count) remain normal. X-ray shows thickening of the soft tissue layer above the radial styloid process of the affected arm.
differential diagnosis. The disease is differentiated from carpal tunnel syndrome, forearm myotendinitis, radiation styloiditis, inflammatory and degenerative diseases of the wrist joint.
Elbow styloiditis - tendovaginitis of the ulnar extensor of the hand, or stenosing ligamentitis of the VI canal of the dorsal carpal ligament, is much less common. Its essence lies in the narrowing of the VI channel due to fibrotic changes in the tendons of the extensor ulnaris of the hand, its sheath and ligaments that form the channel. The cause of the disease is an injury to this area or its long-term professional microtrauma (in seamstresses, typists, polishers, etc.).
Clinic. Spontaneous pains appear in the region of the styloid process of the ulna, aggravated by radial abduction of the hand and radiating to the IV and V fingers. On palpation, there is pain over the styloid process of the ulna, and sometimes a slight swelling in this area. On x-ray, in some cases, a thickening of the soft tissues above the styloid process is found.
differential diagnosis. The disease should be differentiated from Guyon's canal syndrome and osteoarticular diseases of this area.
Tendovaginitis II-V canals of the dorsal ligament in an isolated form are very rare. They usually accompany de Quervain's disease or ulnar styloiditis.
carpal tunnel syndrome. The basis of the disease is tendovaginitis of the flexors of the fingers of the hand or stenosing ligamentitis of the transverse palmar ligament of the wrist. This syndrome is less common than dorsalis ligamentitis because the flexors have stronger tendons than the extensor tendons.
The essence of the disease lies in the development in the canal of a pathological process (inflammatory, traumatic, tumoral nature), which increases intracanal pressure, resulting in the pressure of the branch of the median nerve passing here. As a rule, the tendons of the acid flexors with their thickening are included in the pathological process. and the formation of stenosing tendovaginitis, as well as the transverse ligament itself, where fibrotic changes develop (stenosing ligamentitis).All these processes lead to pressing the branch of the median nerve to the transverse ligament, resulting in the occurrence of sharp pains in the hand.
The causes of carpal tunnel syndrome are primarily trauma to this area, inflammatory diseases of the wrist joint and surrounding tissues, the development of neurinomas, ganglia and other pathological formations, as well as circulatory disorders - venous stasis, vasomotor and humoral disorders that cause ischemia of the median nerve branch.
Clinic. Sharp, burning pains in fingers I-III and the radial side of the fourth finger, aggravated at night and causing insomnia, decreased sensitivity of the fingertips, hand strength, skin changes in the area of three fingers (acrocyanosis or pallor) and a number of trophic disorders in the region of innervation of the median nerve (diffuse swelling of the fingers and hands, increased sweating in this area, erasure of the skin pattern, muscle atrophy), in severe cases - the formation of trophic ulcers on the fingertips (Fig. 60).
On examination, you can find limited swelling and soreness on the palmar surface of the wrist joint (especially in its radial part). Pain in this area is aggravated by flexion and extension of the hand, as well as by squeezing the shoulder with the tonometer cuff for 2 minutes (cuff symptom) or by raising the arm. There is atrophy of the tenor muscles and a decrease in hand strength during dynamometry. X-rays show no abnormalities. The course of carpal tunnel syndrome in traumatic injury can be acute or long-term, chronic. In these cases, after a short rest of the affected limb, all symptoms quickly disappear; in severe cases, persistent contractures of the hand and fingers may develop.
For diagnosis, only the radial half of the palm has a characteristic localization of trophic changes, and this disease is different from the Guyon canal, truncitis tendovaginitis of the dorsal ligament syndrome with a cervical similar clinical picture.
syndrome, the main significance of burning pains, paresthesias and in the first three fingers of the hand and
guyone | transverse |
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(palmar) ligament of the wrist, | wrist, |
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called | Guyon | |||||
located | elbow | |||||
pisiform bone. | Passes through this channel |
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ulnar | and ulnar | artery. When crushing branches |
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ulnar nerve in this canal | (due to trauma, thrombosis |
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ulnar artery, education | ganglion and other reasons) |
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pain, vasomotor | Rice. 60. The area of races and trophic disturbances in |
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innervated distribution of pain and neurobranch | ulnar nerve |
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(IV-V fingers and ulnar side of the palm).
Clinic. Characterized by pain and paresthesia, occurring mainly at night, as well as trophic disorders with their localization in the IV-V fingers and the ulnar surface of the III finger. Pain on palpation and a slight swelling in the pisiform bone, a decrease in the muscle strength of the little finger and atrophy of the hypotenor are noted. This syndrome can be combined with carpal tunnel syndrome, and is rare in isolation.
"Latching" or "springing" finger (Knott's disease). This syndrome occurs due to the development of tendovaginitis of the superficial flexors of the fingers and stenosing ligamentitis of the annular ligaments of the fingers. Its essence lies in the narrowing of the ligamentous canals of the fingers, along which the tendons of the superficial flexors of the fingers pass, due to damage to the tendons themselves, their sheaths and annular ligaments. This process develops as a result of occupational traumatization followed by fibrotic tendon changes in persons whose work is associated with prolonged pressure on the palm and fingers (tailors, polishers, locksmiths, etc.).
The main clinical symptoms are pain at the base, most often of the I, II and IV fingers (one or more) on their palmar surface. The appearance of pain is associated with the movements of the fingers and with pressure on the area of \u200b\u200btheir base. The pain radiates to the hand, sometimes to the forearm. There is stiffness in the fingers in the morning. Palpation reveals soreness on the palmar surface of the metacarpophalangeal joint, and a dense oval nodule (fusiform deformity of the tendon) is also felt here. When bending and unbending the fingers, the patient feels a painful obstacle at the base of the finger, when overcoming which a click is sometimes heard. At this moment, the deformed tendon passes under the ligament. In the future, the sensation of the obstacle increases and can only be overcome with the help of a healthy hand. In the final phase, the finger is fixed in a bent or unbent position.
differential diagnosis. This syndrome must be distinguished from the early phase of Dupuytren's contracture (no clicking or pain), contractures caused by joint diseases (eg, RA), and traumatic contractures.
Tarsal tunnel syndrome develops with tendovaginitis of the posterior tibial muscle and stenosing ligamentitis of the posterior ligamentous canal on the inner surface
sti area of the ankle joint. The syndrome occurs due to compression of the posterior tibial nerve in this canal, which causes a number of vasomotor and trophic disorders of the foot and fingers.
Clinic. There are muscle pains and paresthesias on the medial surface of the foot and in the fingers, as well as fusiform swelling and painful induration of the tissue in this area, accompanied by a violation of pain and tactile sensitivity on the back of the foot. Sometimes the pain syndrome is expressed slightly.
Diagnosis of tendovaginitis and ligamentitis is based on the characteristic localization of the process in thin and long tendons running through the ligamentous channels. Characterized by pain with tension of the tendons, local inflammatory reactions, sometimes vasomotor and trophic disorders, due to compression of the nearby branches of the peripheral nerves.
Treatment. The treatment of tendovaginitis is based on the same principles as the treatment of periarthritis. It must be persistent and complex, especially in de Quervain's disease. Of primary importance is the rest of the affected tendon with the use of splints and removable plaster splints. With professional tendovaginitis, it is advisable to transfer to another job that is not associated with permanent trauma to the affected tendon.
In the acute phase, analgesics are needed, bypassing it - physiotherapeutic procedures - diathermy, paraffin, electrophoresis with analgesics, hydrocortisone phonophoresis, etc.
Carefully begin therapeutic exercises (passive movements). With severe pain and severe inflammation, the affected area is infiltrated with hydrocortisone and novocaine. When the pathological process subsides, physiotherapy and therapeutic exercises are prescribed more actively.
Massage is done very carefully bypassing the affected area. If necessary, they resort to surgical intervention - dissection of the tendon or ligamentous canal, removal of nodules on the tendon, ganglia or neurinomas. Symptomatic treatment in non-severe, recurrent cases can lead to recovery, in more stubborn cases - to contract pdivi and sleep/KcHnio solo work.
BURSITIS AND TENDOBURSITIS
The inflammatory process in serous bags is rarely isolated. It usually accompanies other lesions of the articular or periarticular tissues, most often tendon lesions (tendobursitis). The causes of bursitis are injuries, microtraumatization, as well as the spread of the pathological process to the bags with a number of underlying tissues, articular (with rheumatoid arthritis) and extra-articular (with tendonitis).
Bursae are well-irrigated tissues and therefore are able to quickly respond with an inflammatory reaction to any pathological process that has arisen in neighboring tissues. At the same time, in the bursa there is an effusion of a serous, purulent or hemorrhagic nature and cell proliferation. Subsequently, fibrosis of the walls of the bag develops and the deposition of calcifications in its cavity. Bursitis may be superficial (eg, ulnar or prepatellar bursitis) or deep, under muscle insertions (eg, subdeltoid bursitis).
Clinic. With superficial bursitis, slight pain occurs (sometimes they are absent), a limited elastic, slightly painful swelling appears under the skin. With purulent brown swelling, the swelling can be sharply painful, hot to the touch and covered with hyperemic skin. With calcifying superficial bursitis in the cavity of the bag during palpation, one can feel solid irregularly shaped formations (calcifications). Sometimes focal densifications of the tissue of the bag are palpated, indicating fibrous cicatricial changes in the walls. All this allows to make a diagnosis of superficial
bursitis. It is more difficult to diagnose deep bursitis. In this case, the presence of symptoms of a pathological process in a nearby tendon or joint with restriction of the corresponding movements in it, as well as signs of calcification at the location of the bags, calcification of tendon insertions, periostitis, spurs of the calcaneal bones and other signs of damage to periarticular tissues on the x-ray are important.
There are several variants of bursitis depending on the anatomical localization of the process.
Shoulder bursitis occurs under the deltoid muscle and between the muscles - the short rotators of the shoulder. Most often, subacromial bursitis develops, which is one of the components of humeroscapular periarthritis.
Ulnar bursitis is located superficially between the skin and the olecranon and is characterized by the appearance of a rounded tumor in the elbow area. It develops mainly as a result of professional microtraumatization in draftsmen, engravers, and also as one of the symptoms of the main inflammatory process in systemic diseases of the joints (rheumatoid arthritis, gout, etc.).
Trochanteric bursitis occurs with trochanteritis of the hip joint at the site of attachment of the gluteal muscles to the trochanter as a result of prolonged microtraumatization of this area (in dancers, cyclists, riders), as well as with tuberculous coxitis. Sometimes it is large and then noticeable from the outside when examining the patient.
Ischial bursitis develops between the ischial tuberosity and the gluteus maximus. It is manifested by moderate pain in the ischial tuberosity, aggravated by hip flexion.
Prepatellar burs and t is an inflammatory process in the synovial bag, which is located between the patella and the skin covering it. Most often, this is an independent disease that develops in people whose profession is associated with frequent kneeling (parquet floors, miners, etc.). With the development of bursitis in front of the patella, a large tumor with clear boundaries appears.
Popliteal bursitis (Baker's cyst). A feature of the popliteal serous sac is that in half the cases it connects to the cavity of the knee joint, so in most cases gonarthritis and popliteal bursitis develop simultaneously. The causes of primary popliteal bursitis are injuries, microtraumas, overload of the knee joint (in particular, in violation of statics), secondary - rheumatoid arthritis, gonarthrosis with reactive synovitis and other diseases of the knee joint.
Clinic. Baker's cyst is manifested by moderate pain in the popliteal fossa, aggravated by unbending the lower leg, sometimes by weakness and numbness of the limb (compression of the tibial nerve passing here). The popliteal fossa is filled with a rounded elastic tumor that disappears when the lower leg is bent. Extension of the knee joint is painful and limited. Sometimes the tumor spreads to the upper part of the calf muscle. At a puncture of a cyst receive the transparent liquid reminding synovial. Often there are signs of arthritis of the knee joint at the same time.
Diagnosis. Recognizing a Baker's cyst is difficult. In unclear cases, a cyst puncture with a morphological study of the exudate is necessary. The disease is differentiated from lipoma and hemangioma of the knee joint.
Treatment. It is recommended to reduce the load on the affected area, locally - the use of physiotherapeutic procedures (calcium electrophoresis, hydrocortisone phonophoresis, paraffin applications, etc.), with large or persistent bursitis (non-purulent) - the introduction of hydrocortisone into the periarticular sac, with infectious bursitis - antibiotics. With severe pain and in the presence of calcifications and calcification in the bag, X-ray therapy is indicated. With a torpid course, surgical removal of the bag is necessary.
FASCIITIS AND APONEUROSITIS (FIBROSITIS)
Inflammatory lesions of the fascia and aponeuroses, united by the term "fibrositis", develop mainly under the influence of trauma or professional microtraumatization (mechanical, thermal, chemical, etc.), as well as some common diseases of infectious, toxic, allergic, endocrine and metabolic origin . The vast majority of fasciitis, aponeurositis are independent diseases.
Pathological anatomy. In the initial phase of the disease, a serous-fibrous effusion appears, later fibroblastic proliferation develops with the formation of nodules, and in the final phase of the disease, fibro-scarring changes occur, sometimes with the formation of persistent contractures. Due to the close contact of muscles and fascia, damage to these tissues often occurs simultaneously. Fibromyositis usually develops. At the same time, an inflammatory process with exudation, cell proliferation and sclerotic changes develops in the interstitial tissue of the muscle. The most commonly affected powerful fascia - the wide fascia of the thigh, lumbar and cervical fascia, palmar and plantar aponeurosis.
Clinic. Characterized by slight pain and stiffness in the area of the affected fascia; dense painful nodules appear, which later disappear or, conversely, increase.
Usually, symptoms of myositis are also observed simultaneously - constant pain and tenderness on palpation, uneven muscle consistency, changes in tone and limitation of the function of the affected muscle, muscle contractures and amyotrophy.
With aponeurositis, progressive fibrosis of the aponeurosis comes first, ending in the formation of a contracture, with a sharp limitation of the mobility of the affected area of the aponeurosis. In this case, the pain syndrome is mild, sometimes even absent.
X-rays may show thickening or calcification of the fascia or aponeurosis. There are no laboratory signs of an inflammatory process, but there may be data indicating muscle damage (urinary creatinine excretion, increased activity of muscle enzymes - aldolase, aminotransferase, creatine phosphokinase).
The diagnosis of fasciitis and aponeurositis is made with the appearance of stiffness of the affected area of the fascia and multiple painful nodules, aponeurositis - a significant and progressive compaction of the palmar and plantar aponeuroses with the formation of contractures.
of great value is a biopsy of the affected area with a morphological study of the biopsied tissue. Fasciitis is differentiated mainly from muscle diseases, in which there is a sharp increase in pain with tension of the corresponding muscle and a change in its tone. However, it must be remembered that damage to muscles and fascia is often combined. Fibrous nodules in fasciitis must be distinguished from inflammatory lesions of the subcutaneous adipose tissue (cellulalgia and panniculitis), which are located more superficially and have an elastic consistency.
Fasciitis of the broad fascia of the thigh develops as a result of trauma or professional microtraumatization of the outer surface of the thigh (in porters, carpenters, etc.). Manifested by spontaneous pain and painful nodular compaction in the area of the lateral surface of the thigh. Pain worsens with hip extension and abduction. When the thigh moves, a clicking sound is sometimes heard (sliding of the altered fascia along the surface of the trochanter).
Fasciitis of the lumbar fascia (lumbar fibromyositis) is characterized by the presence of dense painful nodules in the lumbar region and often accompanies chronic lumbago.
Dupuytren's contracture is a chronic inflammatory disease of the palmar aponeurosis (its ulnar part) with progressive fibroscarring changes. The tendons of the IV-V, and sometimes III fingers are usually involved in the process with the gradual formation of a persistent flexion contracture in the metacarpophalangeal and proximal interphalangeal joints (Fig. 61).
Etiology and pathogenesis disease has not been fully elucidated. They attach importance to professional microtraumatization of the palmar aponeurosis in the presence of a hereditary predisposition.
The clinic of the disease is very characteristic: in the palm of the hand, painless pronounced tissue compactions are detected at the base of the IV-V fingers, as well as compaction and shortening of the tendon, which is palpable in the form of very tightly stretched tourniquets. IV and V fingers (sometimes one IV finger) are in a state
Rice. 61. Dupuytren's contracture.
incomplete, and in a late stage and full flexion, tightly adhering to the palmar surface of the hand. Pain is usually absent.
Lederhoz's contracture. It is based on a process similar to that described above, but localized in the region of the outer edge of the plantar aponeurosis. As a result of fibroscarring changes in the aponeurosis and tendons, the fingers are excessively bent, clubfoot and hollow foot develop. Less common are aponeurositis in the area of the flexion surfaces of the elbow and knee joints, where large neurovascular bundles pass. They are manifested by persistent flexion contractures of these joints.
Treatment of fasciitis and aponeurositis should first of all be pathogenetic. It is necessary to ensure the rest of the affected area. Anti-inflammatory therapy is recommended. It is advisable to eliminate the effects of allergies and other possible etiological factors.
For local influence on the pathological process, physical methods of treatment (thermal and electrical procedures), infiltration of the affected area with hydrocortisone, massage, therapeutic exercises, and in some cases surgical intervention (dissection of the fascia, aponeurosis, etc.) are used. At the same time, with myofasciitis, treatment should also be directed to the pathological process in the muscles - the elimination of muscle spasms with the help of muscle relaxants, the improvement of blood circulation in the muscles with the help of vasodilators, and the elimination of pain with the help of analgesics.
- Which doctors should you contact if you have extra-articular rheumatism
What is extra-articular rheumatism
Rheumatic processes in the periarticular tissues refer to extra-articular diseases of the soft tissues of the musculoskeletal system, often combined under the general name "extra-articular rheumatism". This large group of pathological processes of various origins and clinics includes diseases of both tissues located in close proximity to the joints, i.e. periarticular tissues (muscle tendons, their vaginas, mucous bags, ligaments, fascia and aponeuroses), and tissues located at some distance from the joints (muscles, neurovascular formations, subcutaneous fatty tissue).
The most studied are diseases of the periarticular tissues, which have clearly defined localization and clinical manifestations, while RP of soft tissues that are not related to the periarticular ones are characterized by less clear clinical symptoms and often indefinite localization. As a result, in this section we will only touch on diseases of the soft periarticular tissues.
These processes primarily include tendinitis, tendovaginitis, bursitis, tendobursitis, ligamentitis, and also fibrositis.
Diseases of the soft periarticular tissues are very common. In a survey of 6,000 people, they were identified in 8% of individuals. The defeat of the periarticular apparatus occurs more often in women aged 34-54 years, especially in manual workers.
What causes extra-articular rheumatism
Etiology independent diseases of the periarticular tissues is very similar to the etiology of arthrosis. The main cause of these painful syndromes is professional, domestic or sports microtraumatization, which is explained by the superficial location of the soft periarticular tissues and their high functional load. It has been established that long-term repetitive stereotypical movements lead to the development of a degenerative process in tendons, collagen fibers and ligaments, followed by slight reactive inflammation in nearby well-vascularized formations - vaginas and serous sacs. This is evidenced by the frequent development of periarthritis, tendovaginitis, bursitis in athletes, dancers, painters, violinists, typists. Severe physical stress and direct trauma can also cause periarthritis and other soft tissue lesions.
Of great importance are neuroreflex and neurotrophic influences, which worsen the trophism and nutrition of soft periarticular tissues, and contribute to the development of a degenerative process in them. The neuroreflex genesis of such diseases as humeroscapular periarthritis in myocardial infarction, neurotrophic shoulder-hand syndrome, shoulder tendonitis in cervical spondylosis is an established fact.
However, the possibility of developing painful syndromes in the soft periarticular tissues in individuals with a normal load on these tissues (not exceeding the physiological one), in which there is no influence of neuroreflex factors, indicates that there are a number of reasons that reduce the resistance of tissues to the usual physiological load. These primarily include endocrine exchange disorders, as indicated by the frequent development of diseases in women in menopause, especially those suffering from obesity, diseases of the liver and biliary tract. This is evidenced by the frequent combination of periarthritis and arthrosis, which have a similar genesis. As with arthrosis, in this process, the significance of the genetic factor, the congenital weakness of the tendon-ligamentous apparatus or its increased reactivity to the action of various factors that worsen the nutrition and trophism of the periarticular tissues cannot be excluded. The specific mechanisms of the influence of these causes on the development of the degenerative process in periarticular tissues have not yet been studied, but their significance is confirmed by practice.
There are a number of provoking factors contributing to the development of this pathology. The effect of cooling and dampness is well known, which is associated with overstimulation of skin receptors and capillary spasm, which disrupts microcirculation in the periarticular tissues, local metabolism and trophism. Clinical experience shows that a provoking factor in the development of periarticular tissue disease in some cases is a focal infection. In most cases, the occurrence of painful syndromes in the periarticular tissues is the result of a combined effect of several pathogenetic factors.
Pathogenesis (what happens?) during extra-articular rheumatism
Pathogenesis and pathological anatomy. Diseases of the soft periarticular tissues can be inflammatory or degenerative in nature.
Inflammatory diseases of these tissues are most often secondary and result from the spread of the inflammatory process from the joint in arthritis of various origins. Independent, primary diseases of the periarticular tissues are based on a predominantly degenerative process, very similar to that observed in arthrosis. Since the causes of the degenerative process in the articular and periarticular tissues are identical, the simultaneous development of degenerative changes in these tissues is often observed, i.e. arthrosis is often accompanied by periarthritis, tendovaginitis and other lesions of the periarticular apparatus. However, a degenerative process (with subsequent slight reactive inflammation) in the soft periarticular tissues with completely intact joints can also often occur.
The similarity of the pathogenesis of degenerative diseases of the joints and periarticular tissues gives rise to some authors to consider arthrosis and primary disease of the periarticular tissues as clinical variants of a single pathological process.
The primary degenerative process of the periarticular apparatus is most often localized in the tendons (constantly bearing a large load). Due to constant tension and microtrauma in poorly vascularized tendon tissue, ruptures of individual fibrils are observed with the formation of foci of necrosis with hyalinization and calcification of collagen fibers. In the future, sclerosis and calcification of these foci occur, and in nearby well-irrigated synovial formations (vagina, tendons, serous bags), as well as in the tendons themselves, signs of reactive inflammation appear, similar to those that are detected in arthrosis.
The processes described above most often develop at the site of attachment of the tendons to the bone, in the so-called tendon insertions. At the same time, an isolated lesion of the tendon (tendinitis) quickly turns into tendobursitis due to the inclusion of a nearby serous sac in the process. At the same time, due to the reaction of the periosteum, tendoperiostitis develops at the site of contact with it of the affected tendon.
Histologically, in the focus of tendon necrosis, depolymerization of glycosaminoglycans (mucopolysaccharides) is observed with the formation of fibrinoid substance, leukocyte and histiocytic reaction around and subsequent sclerosis and calcification. Most often, insertions of short and wide tendons that carry a large load, such as the tendons of the short shoulder rotators, suffer most often.
With reactive browning in the serous sac, hyperemia, edema with rapid accumulation of serous or purulent exudate in the cavity of the sac is observed. The outcome of this process is mostly favorable: foci of necrosis, exudate and calcifications resolve. However, in some cases, there are residual effects in the form of fibrous fusion of the walls of the bags and the tendon sheath, which makes it difficult for the tendon to slide during its contraction and relaxation and leads to functional disorders.
Although the defeat of synovial formations (synovial sheaths, serous bags) is most often combined with damage to the tendons, however, it can also occur in isolation, sometimes spreading to nearby tendons and causing secondary tendinitis. The degenerative process in the tendons is very often combined with a similar lesion of the ligaments, especially in cases where long and thin tendons pass through narrow ligamentous channels (on the hands and feet). The anatomical relationships here are so close that it is sometimes difficult to resolve the issue of the primacy of the lesion of a particular tissue, i.e., primary tendovaginitis or ligamentitis develops. In these cases, both terms (tendovaginitis and ligamentitis) are often used as synonyms.
The defeat of aponeuroses and wide fascia (fibrositis) is characterized by the predominance of fibrosclerotic processes. They can be widespread (eg, involvement of the entire palmar aponeurosis) or focal (formation of fibrous nodules). In the initial phase, a serous fibrous effusion is observed, which is replaced by a pronounced fibroblastic proliferation with the formation of nodules and subsequent fibroscarring changes, sometimes leading to the formation of persistent contractures.
The variety of pathomorphological changes also causes a large polymorphism of the clinical manifestations of diseases of the periarticular tissues. Thus, the following main processes of periarticular tissues are distinguished.
- Tendinitis is an isolated degenerative lesion of the tendon (with little secondary inflammation). This is usually the first short phase of the degenerative process in the periarticular tissues.
- Tenosynovitis (tenosynovitis) is often the second phase of the pathological process that develops as a result of contact of the affected tendon with well-irrigated synovial tissues.
- Ligamentitis is an inflammatory lesion of extra-articular ligaments; most often the ligamentous canal through which the tendon passes in the area of the wrist and ankle joints.
- Calcification - the deposition of calcium salts in the foci of necrosis and serous bags.
- Bursitis is a local inflammation of the serous sac, most often developing due to contact with the affected tendon (tendobursitis).
- Tendon lesions, in addition, are usually classified according to the predominant localization of the pathological process. The combination of damage to the insertion of the tendon and adjacent formations - the periosteum and serous bag - is called periarthritis. This process most often develops in short and wide tendons that carry a large functional load. The defeat of the middle part of the tendon and its sheath (most often it is thin and long tendons) is referred to as tendovaginitis or tenosipsvit. A lesion localized in the tendon-muscle ligament is called myotendinitis.
- Fasciitis and aponeurositis - diseases of the fascia and aponeuroses - are commonly referred to by the generic term "fibrositis".
Symptoms of extra-articular rheumatism
With lesions of the tendon apparatus, clinical manifestations - pain and limitation of movements - are observed only after the inclusion in the pathological process of synovial formations - the tendon sheath and serous bags. The primary isolated lesion of the tendon itself usually does not show any clinical symptoms. The clinical manifestations of soft periarticular tissue disease have some features that allow for differential diagnosis with joint diseases, which sometimes presents difficulties due to close topography, and sometimes close contact of articular and extra-articular tissues (for example, insertions of muscle tendons and epiphyseal periosteum). The pain that occurs when the tendons are damaged, firstly, arises or intensifies only with movements associated with the affected tendon, while all other movements, due to the intactness of the joint itself and other tendons, remain free and painless. Secondly, they appear only during active movements, when there is tension in the affected tendon. Passive movements due to the lack of contraction of this tendon are painless.
On palpation of the affected area, non-diffuse soreness or soreness along the joint space is determined; as it is observed in diseases of the joints, but local pain points corresponding to the places of attachment to the bone of the insertion of the tendon or the anatomical location of the tendon itself. There is a small and fairly well-defined swelling in the area of the affected tendon or sac (as opposed to diffuse in arthritis).
Localization of periarticular tissue lesions is determined by the intensity of their functional load. The tendons of the hands are mainly affected, which is associated with a multitude and variety of functions of the upper limbs, leading to an almost constant tension of these tendons. Degenerative diseases of the joints are localized, on the contrary, most often in the joints of the legs, which are supporting, therefore, bearing a large functional load.
The most common localization of periarthritis on the upper limb is the area of the shoulder, where the short shoulder rotators and tendons of the biceps muscle are constantly subject to a large functional load, and in difficult conditions (the passage of tendons in a narrow space). This causes the frequent occurrence of tsndoperiostitis of the supraspinatus and infraspinatus muscles, subacromial tendobursitis and tenosynovitis of the long head of the biceps muscle.
In the area of the elbow joint, periarthritis occurs less frequently. Tendoperiostitis usually develops in the area of attachment of the extensor tendons and supinator of the forearm to the external condyle of the shoulder (external epicondylitis). Less commonly, tendobursitis of the tendons attached to the medial condyle of the shoulder (internal epicondylitis) and tendinoperiostitis of the biceps tendon attached to the acromion (acromialgia).
Frequent localization of the degenerative process on the upper extremities are long and thin tendons of the wrist and hand, which pass in narrow fibrous canals. A variety of painful syndromes develop - tendovaginitis of the tendons of the muscles that abduct and extend the thumb (de Quervain's disease), tendovaginitis of the ulnar extensor of the hand (ulnar styloiditis), tendovaginitis of the flexors of the fingers (carpal tunnel syndrome), etc. Damage to the palmar aponeurosis with the development of flexion contracture is much less common. fingers.
On the lower extremities, damage to the tendon apparatus and ligaments is much less common. In the area of the hip joint, tendobursitis of the tendons of the gluteal muscles can develop at the place of their attachment to the large tubercle (trochanteritis) and the iliopsoas muscle at the place of its attachment to the small tubercle.
Tendon bursitis of the tendons develops in the knee area, attaching to the inner surface of the knee and to the tuberosity of the tibia.
The foot and ankle region are the site of the most frequent localization of the degenerative process in the tendons, which, like on the hand, pass through narrow ligamentous canals, as well as at the point of attachment of the Achilles tendon to the calcaneal tuber (achillodynia) and at the point of attachment to the heel bone of the plantar muscles and plantar aponeurosis (with the development of calcaneal bursitis).
The listed lesions of tendons, ligaments and aponeuroses, complicated by the reaction of serous bags and tendon sheaths, can be observed both in isolation and in various combinations.
In 30-40% of patients, radiographs show calcifications along the affected tendon, as well as a periosteal reaction - compaction and small osteophytes at the site of attachment of the tendon to the bone (tendoperiostitis).
Treatment of extra-articular rheumatism
For no other disease there is such a wide choice of therapeutic agents - from rubbing with antirheumatic drugs, ointments based on medicinal plants, ointments with various skin irritating components, the use of heat and cold in a variety of ways, massage, electrotherapy up to acupuncture and other therapeutic techniques. .
Taking antirheumatic drugs is of secondary importance - non-steroidal antirheumatic drugs are widely used here, which suppress pain and inflammation. This does not apply to polymyalgia rheumatica, in which, as we noted above, it is quite characteristic to take anti-inflammatory hormones of the adrenal cortex - corticosteroids (prednisolone). Similarly, pain in diseases of the tendons is treated - by injecting these hormones directly into places where pain is felt.
The most popular medicines for extra-articular rheumatism include therapeutic ointments and solutions (even Sveik in the first chapter of Hasek's book smeared his knees with opedeldoc - a solution containing camphor and mint), that is, substances that cause skin irritation and a reflex increase in blood supply to tissues, which gives a good healing effect. Ointments (thicker than solutions) contain various non-steroidal antirheumatic drugs and are rubbed into the skin until they are absorbed.
An excellent treatment is the local or general use of heat. Heat sources can be a solar lamp, a hot bath with therapeutic additives (solfatan, peat), an electric heating pad, a warm compress or wax applied to the skin, therapeutic mud, including from Piešťany, applied in the form of a tissue compress, which should be “warmed up” at home. » as written in the instructions. Sometimes the patient prefers cold compresses.
Physicians often prescribe electrotherapy treatments such as iontophoresis (injection of drugs into the skin by means of an electric current), diathermy (works with electrical waves, most often short, which are similar to radio waves), ultrasound (an ultrasound device generates a certain high-pitched sound that the human ear does not distinguish it, but the tissues of the body feel its vibrations, and thereby their blood supply increases).
Somewhat more complex are the treatment methods for a sore shoulder. First of all, it is necessary that the doctor determines the cause of the disease. Patience is required here, and one must be aware that in the final stage the result of treatment will always be an improvement, although sometimes it takes several months to wait. During treatment, you should first give preference to rest, not to engage in too active development of the shoulder. The shoulder should be spared, sometimes using a sling for the arm. After the first attack of the disease has passed, the shoulder can be developed with swing movements or with the help of a healthy arm. These exercises are also suitable for other types of rheumatic diseases. It is advisable to first take introductory classes under the guidance of a rehabilitation specialist.
The term soft tissue rheumatism is used to describe symptoms such as severe pain, swelling, or inflammation in the tissues surrounding the joints. These include ligaments, tendons, muscles, bursa, or bursae. In the case of rheumatism of such tissues, from the point of view of medicine, it would be more correct to speak of bursitis or tendonitis and similar pathologies.
Problems with rheumatic soft tissue disorders can be caused by changes in the joints, excessive stress, or a complication after suffering from rheumatoid arthritis. In office workers, inflammatory processes of this nature can be triggered by a long stay in the same position when typing on the keyboard or using the mouse.
Flat feet can create problems in the lower extremities - pain around the heel, ankle, or in the popliteal region. Incorrect positioning of the foot when walking is a common cause of bursitis or pain on the outside of the thigh.
- pain in the shoulder when raising the arm up - inflammation of the tendons (tendinitis);
- pain due to damage to the rotator cuff;
- pain in the hip joint and along the thigh - filling the synovial bag with fluid (bursitis);
- pain in the elbow joint during strenuous activity - tennis elbow;
- tendinitis or bursitis of the knee;
- inflammation of the Achilles tendon, causing heel pain and stiffness when walking;
- inflammation of the tendons of the thumb or wrist - tendovaginitis, most common in young mothers;
- stabbing pains in the thumb - tunnel syndrome;
- inflammation of the shoulder capsule - a frozen shoulder, accompanied by limited mobility and acute pain that worsens at night.
Pain in the muscles and ligaments is called fibromyalgia. This is a common chronic disease that is accompanied by extensive pain, tension or relaxation of muscles and fibrous tissue throughout the body. Severe forms of fibromyalgia in some cases can cause temporary disability and a significant decrease in the patient's quality of life.
People with muscle rheumatism are concerned about symptoms that differ in severity and different localization: in the neck, chest, back, elbows, knees, lower back, etc. Among them are:
- muscle pains of a different nature - cutting, throbbing, burning;
- numbness of the limbs;
- insomnia;
- fast fatigue;
- anxiety, panic attacks;
- headache;
- irritable bowel syndrome;
- depression
- morning muscle stiffness.
Localization of muscle pains of a rheumatic nature along the thigh or in the knee area is a sign of rheumatism of the muscles of the legs. Often these pains are the result of exertion, injury, exposure to dampness, cold, or a systemic rheumatic disease.
For the treatment of fibromyalgia, an integrated approach is used, which includes medication and physiotherapy. The selection of drugs and treatment plan is carried out on an individual basis, depending on the severity of the disease, the age of the patient, his lifestyle and other factors.
For treatment, predominantly non-steroidal anti-inflammatory drugs containing acetaminophen are used - Ibuprofen, Naproxen, Aspirin. Medicines are used only as prescribed by a doctor. Antidepressants and muscle relaxants may also be prescribed. In severe cases, lidocaine is used for pain relief, and corticosteroids are used to relieve inflammation. Physiotherapy includes systematic exercises to maintain muscle strength and elasticity, various types of massage, hot baths, aerobics.
Rheumatic diseases of the periarticular soft tissues- extra-articular lesion of periarticular tissues. Rheumatic diseases of the periarticular soft tissues (extra-articular rheumatism) include inflammatory or degenerative changes in the tendons (tendovaginitis, tendinitis), ligaments (ligamentitis), the area of attachment of ligaments and tendons to the bones (enthesopathy), synovial cavities (bursitis), fascia (fasciitis), aponeuroses (aponeurosis) not associated with trauma, infection, tumor. The main manifestations of this group of rheumatic diseases are pain and difficulty in movement in the joints. Systemic anti-inflammatory therapy is carried out, locally - physiotherapy, the introduction of corticosteroids.
Primary rheumatic diseases include dystrophic and inflammatory lesions of the periarticular structures that occur against the background of intact joints or osteoarthritis. The leading role in their origin is assigned to household, professional or sports loads, as well as endocrine-metabolic, neuro-reflex, vegetative-vascular disorders, congenital inferiority of the ligamentous-tendon apparatus.
In secondary rheumatic diseases, changes in the periarticular tissues are usually caused either by a systemic process (Reiter's syndrome, gouty or rheumatoid arthritis), or by the spread of inflammation from the primary changed joints.
Denoting changes in the periarticular tissues, the terms periarthrosis or periarthritis are sometimes used.
The most common forms of extra-articular rheumatism of the upper limb include humeroscapular, ulnar, radiocarpal periarthritis. Rheumatic lesions of the periarticular tissues of the lower extremity include periarthritis of the hip, knee, and foot. Among other rheumatic diseases of the periarticular soft tissues, zosinophilic fasciitis and fibrositis are considered.
Pathological changes first affect the tendons that are subjected to the greatest load and mechanical stress. This leads to the appearance of fibril defects, foci of necrosis, the development of post-inflammatory sclerosis, hyalinosis and calcification. Primary changes are localized in the places of fixation of the tendons to the bone tissue (enthesis) and are called enthesopathy. In the future, tendon sheaths (tendovaginitis), synovial membranes (bursitis), fibrous capsules (capsulitis), joint ligaments (ligamentitis), etc. may be involved in the process.
Common symptoms of extra-articular rheumatism include pain and limited movement of the joint. Pain is associated with certain active movements in the joint; local painful areas are determined in the areas of fixation of the tendons. With tendovaginitis and bursitis, swelling is clearly detected along the tendons or in the projection of the synovial membrane.
Shoulder-shoulder periarthritis
It mainly develops in women older than 40-45 years. It is caused by dystrophic changes in the tendons of the supraspinatus muscle, rotator muscles of the shoulder (subscapular, infraspinatus, small and large round), tendons of the biceps head (biceps) and subacromial bag.
Interest in the supraspinatus tendons can be expressed as simple tendonitis, calcific tendonitis, tear (or rupture) of the tendon.
Simple tendinitis is characterized by pain in the supraspinatus muscle with active abduction of the arm (Dauborn's symptom), while the greatest pain is noted with an amplitude of abduction of the limb by 70-90 °. A sharp increase in pain is associated with temporary compression of the tendon between the epiphysis of the humerus and the acromion.
The calcific form of tendinitis is diagnosed after performing radiographs of the shoulder joint. Pain symptoms are more pronounced, and the motor function of the joint is more significantly impaired.
A tear or complete rupture of the tendon that fixes the supraspinatus muscle is usually caused by heavy lifting or an unsuccessful fall with emphasis on the arm. It differs from other forms of humeroscapular periarthritis by the typical symptom of a “falling hand”, i.e., the inability to keep the hand in the position laid aside. This condition requires arthrography of the shoulder joint and, if a tendon rupture is detected, surgical intervention.
With tendinitis of the head of the biceps, persistent pain and palpation tenderness are noted when trying to tension the biceps muscle.
The clinic of subacromial bursitis usually develops secondarily, following the defeat of the supraspinatus muscle or biceps. It is characterized by pain, limited rotation and abduction of the limb (symptom of a blocked shoulder). It can occur in the form of calcific bursitis with deposition of calcium salts in the subacromial sac.
Periarthritis of the elbow joint
Options for lesions of the periarticular tissues of the elbow joint include enthesopathy in the area of the epicondyles of the humerus and ulnar bursitis.
Enthesopathies of the tendons fixed to the epicondyle of the shoulder form the pathogenetic basis of the syndrome called "tennis elbow". There are pains in the zone of the external and medial epicondyles of the humerus, which are aggravated by the slightest tension of the extensor and flexor of the hand and fingers.
In the case of ulnar bursitis, a balloting protrusion is determined by palpation in the projection of the olecranon.
Periarthritis of the hip joint
It develops with damage to the tendons of the small and middle gluteal muscles, as well as articular bags in the region of the greater trochanter of the thigh.
For the clinic of hip periarthrosis, the occurrence of pain in the upper outer thighs when walking and absence at rest is typical. Palpation of the soft tissues in the area of the greater trochanter is painful, radiographically revealed calcification of the tendons and osteophytes along the contour of the femoral apophysis.
Periarthritis of the knee joint
It is caused by a lesion of the tendon apparatus, which provides fixation of the semitendinosus, sartorius, slender, semimembranosus muscles to the medial condyle of the tibia. Pain accompanies both active and passive movements (extension, flexion, turn of the lower leg), sometimes there is local hyperthermia and swelling of soft tissue structures.
Therapy of rheumatic lesions of the periarticular soft tissues is carried out by a rheumatologist and includes the appointment of a rest regimen of the limb concerned, medications of the NSAID group (naproxen, butadione, orthophene, indimethacin), phonophoresis sessions with hydrocortisone, exercise therapy, massage.
In the absence of positive dynamics within 2 weeks, a local periarticular blockade of tissues with novocaine or glucocorticosteroids is performed.
With often recurrent or therapy-resistant forms of extra-articular rheumatism, sessions of local radiotherapy are indicated.
