328 SEROrS MEMBEANES. 



more higlil}". It is this latter property \yhicli gives the sclerotic 

 patches of the serous membrane their milky opacity. The essential 

 nature of sclerosis is quite as obscure as that of the processes 

 with which it is associated. As regards these, we do not know 

 whether the transudation is simple or inflammatory ; as regards 

 the sclerosis, whether the hyperplastic change belongs to one or 

 other category. In my opinion we must draw as marked a line 

 as we can between active and passive congestion ; hence we must 

 seek the origin of the disease either in an inflammation, or in a 

 passive disturbance of the circulation. In the majority of cases, 

 our search will be successful. We cannot but admit, however, 

 that passive congestion is a powerful predisposing cause of 

 inflammation ; also, that in everj^ inflammatory hypersemia a 

 statical element is evolved from the unquestionable dilatation of 

 some portion of the circulatory tract. Accordingly, both sets of 

 phenomeim are often intimately associated with one another, and 

 are often so blended that it becomes a matter of the greatest 

 difficulty to determine how much is due to the one, and how 

 much to the other element. Instinctive tact and practical ex- 

 perience are here our best allies. We usually regard the hydro- 

 thorax of valvular disease as a passive transudation, while we 

 take the dropsy of the tunica vaginalis propria testis (hydrocele) 

 to be the type of an inflammatory dropsy. Between these ex- 

 tremes we have dropsy of the pericardium and peritoneum, and 

 dropsy of the ventricles of the brain ; the former more nearly 

 related to hydrothorax, the latter to hydrocele. Efl'usions into 

 bursas mucosae, the synovial sheaths of tendons, and the joints, 

 are a debateable ground. The element of uncertainty, the dis- 

 cretionary element, in this doctrine is due to the absence of 

 available criteria for the determination of the exact point at 

 which the transudation on the one hand, and the morbid gi'owth 

 on the other, should begin to be called inflammatory. Julius 

 Vogel attempted to establish a criterion for the inflammatory 

 nature of the transudation in the presence of spontaneously 

 coagulable albuminous substances {Hydrops fihrinosus^^ inflarn- 

 matorius). But now we know that the fluid which accumulates 

 in the pericardium during the death-struggle, and which cer- 

 tainly is not inflammatory, contains fibrinogen. As regards the 

 morbid product with which we are immediately concerned, an 

 attempt has been made to erect it into an inflammatory forma- 



