But far more arresting are the numerous and well authenticated instances in which local trauma not only determines an outbreak but also its locality. How frequently, too, have blows, strains, sprains, fractures, dislocations, or other trivial or severe injuries, been the signal for an attack. Now, as we hope to show later, local foci of infection are extremely common in the gouty. Such are especially frequent in the teeth, tonsils, naso-pharynx, etc. Is it not then extremely probable that organisms may, viâ the blood-stream, find their way to a joint, the resistance of whose tissues has been lowered by a trauma, however slight its degree? This I apprehend to be the true explanation of the undoubted intimate connection between traumatisms and arthritic outbreaks of gout.
Of similar significance, too, the numerous instances on record in which acute attacks of gout have followed acute tonsillitis, acute pharyngitis, acute parotitis, etc. How frequently, also, competent observers, such as Garrod, noted that boils and carbuncles frequently appeared to be excitant of acute attacks. But to this important point, the intrusion of an infective element in the genesis of gout, we shall return in a later chapter entitled “Gout as an Infection.” It will suffice here if we record our belief that—
(1) Heredity is the sole predisposing factor in gout.
(2) That the differentiation between the usually cited predisposing and exciting causes is unwarrantable.
(3) That both alike are merely determinants.
(4) That their influence as such in exciting outbreaks is exerted through the medium of infection, this achieved either directly or indirectly.
Morbid Anatomy
It has been truthfully affirmed that we know more of the results or products of gout, and less of its essential nature, than of almost any other disease. Thus the post-mortem history of the disorder is concerned almost exclusively with more or less graphic accounts of the uratic deposits, their sites of predilection, and the changes that they induce. Hence it is that the morbid anatomy of gout relates for the most part to its regular or articular manifestations, for it is in and around the joint structures that the deposits for the main part occur.
As to the assumed localisations of the disease in the internal organs, there is no anatomical evidence that they are due to an invasion of the “gouty” inflammation. Not even the renal changes, despite the attestation, as it were, of the gouty process by uratic deposits in the papillæ, can be held as distinctive of gout. Norman Moore found them present in only twelve out of eighty cases. As Osler said, “The presence of uratic concretions at the apices of the pyramids is not a positive indication of gout. They are not infrequent in this country [U.S.], in which gout is rare.... It is not possible to say in a given case that the condition has been due to gout unless marked evidence of the disease co-exists.”
If, then, nothing distinctive can be claimed of the renal, how much less can we construe as “gouty” the anatomical alterations that may or may not be met with in other organs in this disorder. In short, it may be said of the renal as well as the other visceral lesions, so often met with in association with gout, that they are met with even more frequently in its absence, and most certainly fail to attest their “gouty” nature by the appearances which they present.