This theory does not explain all the various and anomalous symptoms of gout, and the question is left unanswered as to why all patients suffering from granular atrophy of the kidneys are not attacked by gout; but it has the advan tage that it brings into one category all the etiological and pathogenic factors with which we are acquainted, and gives a plausible explanation of the origin of gout as well of the rich and overfed classes as of the poor and badly nour ished. By this theory the close alliance of uric-acid gravel with gout becomes intelligible, and the enigmatic gout caused by lead impregnation has a ra tional explanation.
Pathology. — The most characteristic pathological change found in gout is the presence of deposits of biurate in various tissues. The order of invasion is fairly constant: the diarthrosial cartilages are the first to be affected; then the liga ments, tendons, and bursa',; next the con nective tissue and the skin become im pregnated. Of the articulations the metatarso-phalangeal joint of the great toe is generally first affected, then the different metatarso- and metacarpo- pha langeal articulations, the tarsus and carpus, and next the larger joints; but their order is not constant. Almost all joints are attacked by gout,—perhapa with the exception of the hip-joint. The deposit first occurs in the superficial part of the cartilage close under its surface, in the form of fine, crystalline needles forming a more or less close net-work and presenting different degrees of opacity; sometimes it may be so small as to require the aid of a microscope for its detection. At first the central parts of the cartilages only are impregnated, whereas the peripheral tissues are free from deposits, but present some vascu larization. Subsequently the fibrocar tilages, ligaments, and synovial mem branes become involved with white chalk-line deposits consisting of biurate; the synovial fluid may also contain crys tal needles. The articulations become stiffened or fixed and ultimately they are greatly distorted and nodulated. The skin covering the affected joint becomes distended, and it may even be destroyed, exposing chalky masses, which break down and are successively evacuated, frequently giving rise to suppurative and ulcerative processes of the skin. It does not mean that the deposit is specially in filtrated in the cells, but rather that it pushes its way without special regard as to the component elements of the car tilage.
The periosteum and bursar may also be implicated, and some authors have even believed that the bone itself may become affected. Virchow has described isolated infiltrations of biurates in the spongy tissue of the phalanges, and in the marrow of the bones deposits may occur, mostly, but not always, in the neighborhood of incrusted cartilages.
Marchand and Lehmann have made chemical analysis of bone-tissue of gouty patients, and found that when the car tilages and the periosteum were removed the osseous tissue itself did not contain uric acid. Garrod observed that in gout of long standing the osseous tissue of the phalanges may become rarefied and the vacuoles filled with fat; by this process the bones are rendered more fragile than in the normal state.
Heberden observed a knotty or bosse lated condition of the terminal phalan geal joints; this pathological state of the fingers has been known as Heberden's finger. In Heberden's opinion, the knots are not of gouty origin, but caused by arthritis deformans; a similar formation of the phalanges may, however, also be observed in gouty patients in very ad vanced life.
Deposits may be found in various other parts of the body, such as the ex ternal ear, eyelid, nose, and larynx; they form there nodules—tophi—which at first contain a liquid, but after some time get hard. Garrod evacuated from a single tophus of the hand 60 grammes (2 ounces) of biurate.
The muscles of gouty patients are or dinarily atrophic, especially when the extremities get stiffened and immovable.
The heart is frequently hypertrophic; myocarditis may occur, leading to the formation of fibroid or fatty degenera tion of the muscles. The endocardium is sometimes in a state of chronic in fl•nmation. and uratic deposits have been observed in it. fn the aorta arte riosclerotic changes and uratic deposits have been noticed.
In the concretions in sclerosed aortic valves urates can sometimes be demon strated by the murexide reaction, along with calcium phosphate and carbonate. More frequently gout causes valvular lesions indirectly as the result of sclerotic changes, but in this process other factors, such as abuse of alcohol or tobacco, lues, or overeating, assist. Gout is more prone to cause motor and sensory cardiac neu roses. Beginning with palpitation, soon followed by tachycardia, dilatation of the ventricles develops, with all its con - sequences. The sensory disturbances vary from mild, pricking pain in the region of the apex or more severe radi ating pains to paroxysmal pain, with tenderness on pressure over the sternum or the base of the heart. The latter con dition is often associated with symptoms of heart-weakness and can lead to angina pectoris. The prognosis in pure cases, not too far advanced, is good under proper treatment. Th. Schott (Berliner klin. \Voch., Nos. 21 and 23, '96).