182 FRANKLIN C. McLEAN 



This pressure tends to drive the fluid, together with its dissolved substances, 

 through such membranes as are permeable to it and with which it comes 

 in contact. Hydrostatic pressure was originally considered by Ludwig(a) 

 to be the essential factor in lymph formation, and this conception is still 

 strongly supported by numerous authors. According to Ludwig, the 

 hydrostatic pressure in the capillaries is higher than in the tissues, and 

 under the influence of this pressure filtration of fluid occurs from the 

 capillaries out into the tissue spaces. The process might be compared 

 with the flow of a solution of sodium chlorid through folded filter paper, 

 as a result of the pressure of the solution in contact with the paper. The 

 rate of filtration, in this case, depends on the pressure of the fluid, its 

 physical properties, and on the permeability of the filter. Starling (a.) (&) 

 considers filtration to be the most important factor in the process of lymph 

 production in regions of the body where the capillary walls are fairly 

 permeable, as in the abdominal regions. 



On the basis of filtration, edema may be explained as due to an in- 

 creased rate of filtration, dependent upon the hydrostatic effect of in- 

 creased capillary pressure, or upon increased permeability of the capillary 

 walls. Increased permeability is then due either to mechanical injury, 

 increased intracapillary pressure, the toxic effect of accumulated products 

 of tissue metabolism, other poisons, or the injurious effects of lack of 

 nourishment. 



According to the majority of the supporters of the filtration theory, 

 there is passage of fluid outward from the arterial end of the capillaries, a 

 current of fluid in the tissue spaces toward the venous end of the capil- 

 laries, and a reabsorption of fluid at the venous end. The source of energy 

 for the flow of fluid is the hydrostatic pressure in the arterial end of the 

 capillaries, and the gradient is provided by the diminishing pressure 

 toward the venous end of the capillaries. It is necessary to assume that 

 the pressure in the capillaries falls more rapidly than it does outside of 

 them, and that there is actually a difference in pressure maintained 

 between the contents of the capillaries and the tissue fluids. Hill (1906), 

 however, has pointed out that it is impossible to conceive of a constantly 

 maintained difference in hydrostatic pressure on the two sides of the 

 capillary wall, when fluid is passing freely through such a wall. 



There is very little evidence that increased capillary pressure has to 

 do with the production of edema. In fact, the occurrence of edema does 

 not parallel increase in venous pressure, even in heart failure (Volhard), 

 and there is no evidence of increased capillary or venous pressure in 

 chronic parenchymatous nephritis, the condition in which edema is an 

 almost constant phenomenon. 



Cohnheim, Magnus, and others have strongly supported the theory 

 of edema as a- result of increased permeability of the capillaries, due to 

 increased carbon dioxid, lack of oxygen, poisons from the infection re- 



