INFLAMMATORY EDEMA 351 



supRest. Kunijif, indeed, often found more chlorides in edematous fluids of non- 

 nephritic origin than in nephritic edema.'*' Fischer holds that the retention 

 of chlorides in edema is secondary and not primary, for he found that tissues 

 made to take up more water through acidification, also take up an increased 

 amount of chlorides. 



Inflammatory Edema. — Although here the alterations in the cap- 

 illary walls play an essential role, as shown by the protein-rich na- 

 ture of the exudates, yet most of the other factors are added. In- 

 creased blood pressure is prominent; lymph outflow is impeded by 

 plugging of the lymphatic channels by clots and leucocytes, and by 

 pressure on the outside; there is, undoubtedly, an excessive forma- 

 tion of metabolic products in the tissues, to cause exosmosis, and the 

 asphyxial conditions in inflamed tissues favor acid formation which 

 ma}' cause in the colloids an increased affinity for water. According 

 to Oswald'*^ the permeability of the vessels for proteins becomes spe- 

 cifically altered in inflammation, so that not only the less viscous 

 albumin and pseudoglo])uhn pass through their walls, but also the more 

 viscous euglobulin and fibrinogen. To this class of edemas belong 

 also the urticarias which follow the ingestion of various toxic sub- 

 stances, many of which can be shown experimentally to be lympha- 

 gogues. A good example is the urticaria which often follows the 

 injection of antitoxic or other foreign serums, particularly their re- 

 peated injection; in experimental animals such a serum may cause 

 death very quickly by acute pulmonary edema. All these poisons 

 probably produce urticarial edema by injury to the capillary walls in 

 the subcutaneous tissues, and possibly changes in the hydrophilic 

 properties of the tissue colloids are also produced by the poisons. In 

 the action of vesicants especially, it may well be questioned if changes 

 in the capillary walls and active hyperemia are not supplemented by 

 local metabolic alterations. The edema which follows the sting of 

 insects, which are known to secrete into the wound such acids as 

 formic, seems to be a particularly good illustration of the production 

 of edema by the influence of acids on the tissues (Fischer). 



Neuropathic Edema. — Until we understand better than we now 

 do the manner in which nervous impulses modify metabolism, it will 

 be difficult to estimate properly the importance of nervous impulses 

 in the production of edema. That nervous control is a possible factor 

 is well shown by manj^ experiments; for example, simple ligation of 

 the femoral vein in animals does not cause edema, but if the sciatic 

 nerve is cut the vasoconstrictors are paralyzed, and edema mav follow 

 (Ranvier).^^ In this case the nervous influence is only indirect 

 through its vasomotor effects. Similarly, stimulation of vasodilator 



*^ Breitmann (Zentr. inn. Med., 1913 (34), 633) describes under the name of 

 "soda dropsy" a form of edema which results from excessive administration of 

 sodium bicarbonate to correct acidosis in diabetes. 



" A. Oswald, Zeit. exp. Path., 1910 (8), 226. 



*^ Similarly, pulmonary edema follows experimental hydremia onlj- when the 

 vagi are cut (F. Kraus, Zeit. exp. Path., 1913 (14), 402). 



