GOUT -MORBID ANATOMY.
The deformation and destruction of the joints that take place in chronic gout furnish a picture with which the earliest of investiga tors were only too familiar. The ancient writers were careful observ ers, and many of their descriptions of the macroscopic appearance produced by the disease are as perfect as anything that has since been recorded. The chalky deposits that infiltrate the joints were, how ever, regarded as something uncommon, and only to be found in chronic and inveterate cases of the disease. They were supposed to represent the " peccant humors" that filtered drop by drop into the cavity of the affected joint, until it could hold no more, and over flowed into the adjacent tissues.
The great merit of Sir A. Garrod's researches lay in his demon stration of the fact that the urates, which compose the bulk of these deposits, were not absent from the articular tissues in cases of acute and recent gout—even when no external evidence of infiltration could be detected. To his investigations is due the proof that in every case of articular gout uratic infiltration is the primitive and all-important fact.
When a gouty joint from a patient in an early stage of the dis ease is laid open for inspection, the first thing that fixes the attention is the change that is exhibited by the diarthrodial surfaces. Instead of the uniformly smooth and yellowish-white surface presented by the cartilaginous investment of healthy bones, there are visible, here and there, stains and streaks and spots of a dull clayey-white, imbedded in the substance of the cartilages. The superficial layer of pavement cells is not involved at this early period of infiltration, and the articu lation still retains its normal shape and function. But as the disease progresses the process of infiltration advances, until the entire carti lage at the end of the bone is transformed into a uniformly clayey white substance occupied by a deposit of sodium urate. The su perficial layer is now attacked, and the articular surface becomes roughened by the destruction of the endothelial layer.
These erosions become deeper and wider, and irregular protru sions of inflammatory tissue that has become saturated with unites encroach on the cavity of the joint. In aggravated cases the original diarthrodial structures disappear, and the roughened ends of the bones project into an irregular cavity that is filled with a semifluid substance that resembles a mixture of plaster-of-Paris and water before it has solidified. The capsule of the joint and its component ligaments and tendons are also in like manner saturated with mineral matter, which is sometimes thus accumulated in great quantity, to the utter deformation and ruin of the affected part.
The location of this morbid process is not an accidental affair.
The small joints of the extremities are the favorite points of attack. The frequency with which the articulations of the great toe are in vaded in cases of typical gout has always arrested attention. Next in order come the metatarso- and metacarpo-phalangeal articula tions; then the joints at the ankle and the wrist.
The larger articulations of the upper and lower extremities, and of the vertebral column, are less liable to invasion, and when they suf fer, the progress of the disease from the periphery toward the cen tre is less regularly marked. Occasionally, however, some of the large joints are diseased, while the smaller joints of the hand and wrist remain entirely free from infiltration. As a general rule the extent and the severity of the lesions are proportionate to the fre quency and the intensity of the local attacks of the disease; but sometimes it happens that post-mortem examination reveals charac teristic changes in articulations that had never been suspected of disorder during the life of the patient.
Au interesting fact that may be noted in this connection is the manner in which the diarthrodial infiltration progresses. It is not at the periphery of the joint that the characteristic clay-colored spot appears at the commencement of the process; it is in the central por tion of the cartilaginous expanse that the primitive lesion is dis coverable. Here is the most conspicuous area of change, while the peripheral portions of the articular surface exhibit only insignificant streaks and spots of disease. Since the regions thus primitively involved are the farthest removed from the network of nutrient capil laries that feed the diarthrodial structures, it is highly probable that the cause of this selection lies in the comparative absence of circula tion and the more easily retarded nutrition that must characterize such territories. It is also probable that the direct effect of superior pressure upon certain portions of the cartilages may act as a deter mining cause. The well-known fact that a gouty attack may be pre cipitated by a long walk, a dance, or any other event that necessitates unusual compression of the joint surfaces, lends additional color to this hypothesis. Wherever circulation and nutrition are retarded, a crystalline deposit of sodium urate will be more easily effected. For this reason the process of infiltration is at an early period manifested at the points of insertion of the lateral and inter-articular ligaments; so that when the joint is laid open the clay-like deposit that occupies the centre of the cartilage is separated by a considerable healthy space from the streaks and smaller patches that mark the ligamentous struc ture in the capsular wall of the articulation.