Pyogenic Diseases

The commoner pyogenic diseases are the result of infection of one or other of the joint structures with staphylococci or streptococci, which may be demonstrated in the exudate in the joint and in the substance of the synovial membrane. The mode of infection is the same as in the pyogenic diseases of bone, the metastasis occurring most frequently from the mucous membrane of the pharynx (J. B. Murphy). The localisation of the infection in a particular joint is determined by injury, exposure to cold, antecedent disease of the joint, or other factors, the nature of which is not always apparent.

The effects on the joint vary in severity. In the milder forms, there is engorgement and infiltration of the synovial membrane, and an effusion into the cavity of the joint of serous fluid mixed with flakes of fibrin—serous synovitis. In more severe infections the exudate consists of pus mixed with fibrin, and, it may be, red blood corpuscles—purulent or suppurative synovitis; the synovial membrane and the ligaments are softened, and the surface of the membrane presents granulations resembling those on an ulcer; foci of suppuration may develop in the peri-articular cellular tissue and result in abscesses. In acute arthritis, all the structures of the joint are involved; the articular cartilage is invaded by granulation tissue derived from the synovial membrane, and from the marrow of the subjacent bone; it presents a worm-eaten or ulcerated appearance, or it may undergo necrosis and separate, exposing the subjacent bone and leading to disintegration of the osseous trabeculæ—caries. With the destruction of the ligaments, the stability of the joint is lost, and it becomes disorganised.

The clinical features vary with the extent of the infection. When this is confined to the synovial and peri-synovial tissues—acute serous and purulent synovitis—there is the usual general reaction, associated with pyrexia and great pain in the joint. The part is hot and swollen, the swelling assuming the shape of the distended synovial sac, fluctuation can usually be elicited, and the joint is held in the flexed position.

When the joint is infected by extension from the surrounding cellular tissue, the joint lesion may not be recognised at an early stage because of the swollen condition of the limb, and because there are already symptoms of toxæmia. We have observed a case in which both the hip and knee joints were infected from the cellular tissue.

If the infection involves all the joint structures—acute arthritis—the general and local phenomena are intensified, the temperature rises quickly, often with a rigor, and remains high; the patient looks ill, and is either unable to sleep or the sleep is disturbed by starting pains. The joint is held rigid in the flexed position, and the least attempt at movement causes severe pain; the slightest jar—even the shaking of the bed—may cause agony. The joint is hot, tensely distended, and there may be œdema of the peri-articular tissues or of the limb as a whole. If the pus perforates the joint capsule, there are signs of abscess or of diffuse suppuration in the cellular tissue. The final disorganisation of the joint is indicated by abnormal mobility and grating of the articular surfaces, or by spontaneous displacement of the bones, and this may amount to dislocation. In the acute arthritis of infants, the epiphysis concerned may be separated and displaced.

When the joint is infected through an external wound, the anatomical features are similar to those observed when the infection has reached the joint by the blood-stream, but the destructive changes tend to be more severe and are more likely to result in disorganisation.

The terminations vary with the gravity of the infection and with the stage at which treatment is instituted. In the milder forms recovery is the rule, with more or less complete restoration of function. In more severe forms the joint may be permanently damaged as a result of fibrous or bony ankylosis, or from displacement or dislocation. From changes in the peri-articular structures there may be contracture in an undesirable position, and in young subjects the growth of the limb may be interfered with. The persistence of sinuses is usually due to disease in one or other of the adjacent bones. In the most severe forms, and especially when several joints are involved, death may result from toxæmia.

The treatment is carried out on the same principles as in other pyogenic infections. The limb is immobilised in such an attitude that should stiffness occur there will be the least interference with function. Extension by weight and pulley is the most valuable means of allaying muscular spasm and relieving intra-articular tension and of counteracting the tendency to flexion; as much as 15 or 20 pounds may be required to relieve the pain.

The induction of hyperæmia is sometimes remarkably efficacious in relieving pain and in arresting the progress of the infection. If the fluid in the joint is in sufficient quantity to cause tension, if it persists, or if there is reason to suspect that it is purulent, it should be withdrawn without delay; an exploring syringe usually suffices, the skin being punctured with a tenotomy knife, and, as practised by Murphy, 5 to 15 c.c. of a 2 per cent. solution of formalin in glycerin are injected and the wound is closed. In virulent infections the injection may be repeated in twenty-four hours. Drainage by tube or otherwise is to be condemned (Murphy). A vaccine may be prepared from the fluid in the joint and injected into the subcutaneous cellular tissue.

Suppuration in the peri-articular soft parts or in one of the adjacent bones must be looked for and dealt with.

When convalescence is established, attention is directed to the restoration of the functions of the limb, and to the prevention of stiffness and deformity by movements and massage, and the use of hot-air and other baths.

At a later stage, and especially in neglected cases, operative and other measures may be required for deformity or ankylosis.