PATIiaCESESIS OF EDEMA 341 



Another way in which i'(hMna may \)v caused oi- infhienced by 

 lymphatic obstruction is generally overlooked, but it is possibly of 

 great importance; namely, from pressure upon the lymph channels by 

 dilated vessels in hyperemia, or by cellular exudates and swollen 

 tissues in inflammation. We see evidence of this in the rapid absorp- 

 tion of exudates that frequentl}- follows the removal of but a part of 

 the fluid in a chest cavity; apparently the decrease in pressure frees 

 the paths of absorption and permits them to take up the remaining 

 fluid. In inflammatory edema the lymphatic obstruction is probably 

 not great, for Lassar found that the amount of lymph escaping from 

 an edematous extremity is much greater than from a normal one; 

 but in the case of strangulated hernias or other conditions in which 

 edema results from circular constriction, obstruction of the h^mphatic 

 vessels may be a factor of no mean importance. In general stasis the 

 increased pressure in the veins of the neck may interfere with the 

 passage of the fluid out of the thoracic duct into the blood. 



There is no difficulty in understanding edema from the above 

 causes — it is simply a passive congestion of the lymphatic circulation, 

 and no chemical factors are involved. The nature of the fluid found in 

 such forms of edema will be discussed later. 



2. Increased Blood Pressure. — This takes us back to the filtra- 

 tion theory of lymph formation, and as it is generally conceded that 

 more or less fluid escapes from the vessels by this mechanical process, ^^ 

 the questions to be decided are: Can and does increased blood pres- 

 sure, alone and wdthout other aiding factors, cause edema? If not, 

 does it play an auxiliarj^ part in producing edema, and how important 

 a part may this be? Many experiments have been performed with the 

 object of answering these questions, with more or less conflicting re- 

 sults. Cohnheim demonstrated that vasodilation (active hyperemia) 

 alone will never bring on an edema; and many observers state that 

 ligation of the femoral or other large veins will not cause edema in 

 animals. However, when the vein is occluded, and the arteries are 

 dilated by cutting their vasoconstrictor nerves, then edema may result 

 (Ranvier, Cohnheim); but whenever venous outflow is impeded, we 

 have other factors than simply increased pressure to consider, for the 

 nourishment of the parts is decidedly impaired, and, as we shall see 

 later, this may be of much greater importance than is the associated 

 rise in blood pressure. To produce edema in the lungs by mechanical 

 forces it is necessary to ligate the aorta and its branches, or the pul- 

 monary veins (Welch), As such high pressures do not occur in any 

 pathological concHtions, it is safe to assume that increased pressure 

 alone is not capable of causing by itself the pulmonarj^ edema so fre- 

 quently observed clinically. Welch, ^^ however, has supported the 



^^ A rise of blood pressure leads to an increase in the hemoglobin of the blood, 

 presumably because the fluid is forced out into the tissue spaces (Scott, Amer. 

 Jour. Physiol., 1917 (44), 298). 



" Virchow's Arch., 1878 (72), 375; see also Meltzer {loc. cit.). 



