Manual of Surgery - Alexis Thomson (read me a book txt) 📗
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The treatment—besides that of the urethral disease or of the ophthalmia—consists in rest until all pain and sensitiveness have disappeared. The pain is relieved by salicylates, but most benefit follows weight extension, the induction of hyperæmia by the rubber bandage and hot-air baths; if the joint is greatly distended, the fluid may be withdrawn by a needle and syringe. Detoxicated vaccines should be given from the first, and in afebrile cases the injection of a foreign protein, such as anti-typhoid vaccine, is beneficial (Harrison).
Murphy has found benefit from the introduction into the joint, in the early stages, of from 5 to 15 c.c. of a 2 per cent. solution of formalin in glycerin. This may be repeated within a week, the patient being kept in bed with light weight extension. In the chronic hydrops the fluid is withdrawn, and about an ounce of a 1 per cent. solution of protargol injected; the patient should be warned of the marked reaction which follows.
After all symptoms have settled down, but not till then, for fear of exciting relapse or metastasis, the joint is massaged and exercised. Stiffness from adhesions is most intractable, and may, in spite of every attention, terminate in ankylosis even in cases where there has been no suppuration. Forcible breaking down of adhesions under anæsthesia is not recommended, as it is followed by great suffering and the adhesions re-form. Operation for ankylosis—arthroplasty—should not be undertaken, as the ankylosis recurs.
Tuberculous DiseaseTuberculous disease of joints results from bacillary infection through the arteries. The disease may commence in the synovial membrane or in the marrow of one of the adjacent bones, and the relative frequency of these two seats of infection has been the subject of considerable difference of opinion. The traditional view of König is that in the knee and most of the larger joints the disease arises in the bone and in the synovial membrane in about equal proportion, and that in the hip the number of cases beginning in the bones is about five times greater than that originating in the membrane. This estimate, so far as the actual frequency of bone lesions is concerned, has been generally accepted, but recent observers, notably John Fraser, do not accept the presence of bone lesions as necessarily proving that the disease commenced in the bones; he maintains, and we think with good grounds, that in many cases the disease having commenced in the synovial membrane, slowly spreads to the bone by way of the blood vessels and lymphatics, and gives rise to lesions in the marrow.
Morbid Anatomy.—Tuberculous disease in the articular end of a long bone may give rise to reactive changes in the adjacent joint, characterised by effusion and by the extension of the synovial membrane over the articular surfaces. This may result in the formation of adhesions which obliterate the cavity of the joint or divide it into compartments. These lesions are comparatively common, and are not necessarily due to actual tuberculous infection of the joint.
The infection of the joint by tubercle originating in the adjacent bone may take place at the periphery, the osseous focus reaching the surface of the bone at the site of reflection of the synovial membrane, and the infection which begins at this point then spreads to the rest of the membrane. Or it may take place in the central area, by the projection of tuberculous granulation tissue into the joint following upon erosion of the cartilage (Fig. 156).
Fig. 156.—Section of Upper End of Fibula, showing caseating focus in marrow, erupting on articular surface and infecting joint.
Changes in the Synovial Membrane.—In the majority of cases there is a diffuse thickening of the synovial membrane, due to the formation of granulation tissue, or of young connective tissue, in its substance. This new tissue is arranged in two layers—the outer composed of fully formed connective or fibrous tissue, the inner of embryonic tissue, usually permeated with miliary tubercles. On opening the joint, these tubercles may be seen on the surface of the membrane, or the surface may be covered with a layer of fibrinous or caseating tissue. Where there is greater resistance on the part of the tissues, there is active formation of young connective tissue which circumscribes or encapsulates the tubercles, so that they remain embedded in the substance of the membrane, and are only seen on cutting into it.
The thickened synovial membrane is projected into the cavity of the joint, filling up its pouches and recesses, and spreading over the surface of the articular cartilage “like ivy growing on a wall.” Wherever the synovial tissue covers the cartilage it becomes adherent to and fused with it. The morbid process may be arrested at this stage, and fibrous adhesions form between the opposing articular surfaces, or it may progress, in which case further changes occur, resulting in destruction of the articular cartilage and exposure of the subjacent bone.
In rare instances the synovial membrane presents nodular masses or lumps, resembling the tuberculous tumours met with in the brain; they project into the cavity of the joint, are often pedunculated, and may give rise to the symptoms of loose body. The fringes of synovial membrane may also undergo a remarkable development, like that observed in arthritis deformans, and described as arborescent lipoma. Both these types are almost exclusively met with in the knee.
The Contents of Tuberculous Joints.—In a large proportion of cases of synovial tuberculosis the joint is entirely filled up by the diffuse thickening of the synovial membrane. In a small number there is an abundant serous exudate, and with this there may be a considerable formation of fibrin, covering the surface of the membrane and floating in the fluid as flakes or masses; under the influence of movement it may assume the shape of melon-seed bodies. More rarely the joint contains pus, and the surface of the synovial membrane resembles the wall of a cold abscess.
Ulceration and Necrosis of Cartilage.—The synovial tissue covering the cartilage causes pitting and perforation of the cartilage and makes its way through it, and often spreads widely between it and the subjacent bone; the cartilage may be detached in portions of considerable size. It may be similarly ulcerated or detached as a result of disease in the bone.
Caries of Articular Surfaces.—Tuberculous infiltration of the marrow in the surface cancelli breaks up the spongy framework of the bone into minute irregular fragments, so that it disintegrates or crumbles away—caries. When there is an absence of caseation and suppuration, the condition is called caries sicca.
The pressure of the articular surfaces against one another favours the progress of ulceration of cartilage and of articular caries. These processes are usually more advanced in the areas most exposed to pressure—for example, in the hip-joint, on the superior aspect of the head of the femur, and on the posterior and upper segment of the acetabulum.
The occurrence of pathological dislocation is due to softening and stretching of the ligaments which normally retain the bones in position, and to some factor causing displacement, which may be the accumulation of fluid or of granulations in the joint, the involuntary contraction of muscles, or some movement or twist of the limb. The occurrence of dislocation is also favoured by destructive changes in the bones.
Peri-articular tubercle and abscess may result from the spread of disease from the bone or joint into the surrounding tissues, either directly or by way of the lymphatics. A peri-articular abscess may spread in several directions, sometimes invading tendon sheaths or bursæ, and finally reaching the skin surface by tortuous sinuses.
Reactive changes in the vicinity of tuberculous joints are of common occurrence, and play a considerable part in the production of what is clinically known as white swelling. New connective tissue forms in the peri-articular fat and between muscles and tendons. It may be tough and fibrous, or soft, vascular, and œdematous, and the peri-articular fat becomes swollen and gelatinous, constituting a layer of considerable thickness. The fat disappears and is replaced by a mucoid effusion between the fibrous bundles of connective tissue. This is what was formerly known as gelatinous degeneration of the synovial membrane. In the case of the wrist the newly formed connective tissue may fix the tendons in their sheaths, interfering with the movements of the fingers. In relation to the bones also there may be reactive changes, resulting in the formation of spicules of new bone on the periosteal surfaces and at the attachment of the capsular and other ligaments; these are only met with where pyogenic infection has been superadded.
Terminations and Sequelæ.—A natural process of cure may occur at any stage, the tuberculous tissue being replaced by scar tissue. Recovery is apt to be attended with impairment of movement due to adhesions, ankylosis, or contracture of the peri-articular structures. Caseous foci in the interior of the bones may become encapsulated, and a cure be thus effected, or they may be the cause of a relapse of the disease at a later date. Interference with growth is comparatively common, and may involve only the epiphysial junctions in the immediate vicinity of the joint affected, or those of all the bones of the limb. This is well seen in adults who have suffered from severe disease of the hip in childhood—the entire limb, including the foot, being shorter and smaller than the corresponding parts of the opposite side.
Atrophic conditions are also met with, the bones undergoing fatty atrophy, so that in extreme cases they may be cut with a knife or be easily fractured. These atrophic conditions are most marked in bedridden patients, and are largely due to disuse of the limb; they are recovered from if it is able to resume its functions.
Clinical Features.—These vary with the different anatomical forms of the disease, and with the joint affected.
Sometimes the disease is ushered in by a febrile attack attended with pains in several joints—described by John Duncan as tuberculous arthritic fever. This is liable to be mistaken for rheumatic fever, from which, however, it differs in that there is no real migration from joint to joint; there is an absence of sweating and of cardiac complications; and no benefit follows the administration of salicylates.
In exceptional cases, tuberculous joint disease follows an acute course resembling that of the pyogenic arthritis of infants. This has been observed in children, especially in the knee, the lesion being in the synovial membrane, and attended with an accumulation of pus in the joint. If promptly treated by incision and drainage, recovery is rapid, and free movement of the joint, may be preserved.
The onset and early stages of tuberculous disease, however, are more often insidious, and are attended with so few symptoms that the disease may have obtained a considerable hold before it attracts notice. It is not uncommon for patients or their friends to attribute the condition to injury, as it often first attracts attention after some slight trauma or excessive use of the limb. The symptoms usually subside under rest, only to relapse again with use of the limb.
The initial local symptoms may be due to the presence of a focus in the neighbouring bone, perhaps causing neuralgic pains in the joint, or weakness, tiredness, stiffness, and inability to use the limb, these symptoms improving with rest and being aggravated by exertion.
It is rarely possible by external examination to recognise deep-seated osseous foci in the vicinity of joints; but if they are near the surface in a superficial bone—such as the head of the tibia—there may be local thickening of the periosteum, œdema, pain, and tenderness on pressure and on percussion.
X-ray Appearances of Tuberculous Joints.—Gross lesions such as caseous foci in the marrow of
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