The plasma colloid osmotic pressure is often low in alcoholics with chronic liver disease (cirrhosis). The diseased liver cannot produce adequate amounts of albumin, which leads to a decrease in the concentration of albumin in the plasma, i.e., hypoalbuminemia. Because about 75% of the plasma colloid osmotic pressure can be attributed to the presence of albumin in the plasma, the decrease in plasma albumin concentration that occurs in the latter stages of cirrhosis often leads to peripheral edema. Cirrhosis also causes excess fluid to accumulate in the peritoneal cavity as ascites. In the case of ascites, the edema results not only from hypoalbuminemia, but also from poal vein obstruction (which increases capillary hydrostatic pressure) as well as the obstruction of lymphatic drainage of the liver. In fact, ascites is observed more often than peripheral edema in liver disease. A decrease in capillary hydrostatic pressure would tend to decrease fluid loss from the capillaries, and thereby oppose the development of edema. A decrease in the colloid osmotic pressure of the interstitial fluid would decrease fluid loss from the capillaries, thereby opposing the development of edema. A decrease in interstitial hydrostatic pressure would tend to increase fluid loss from the capillaries, but this cannot be considered a primary cause of edema because the interstitial hydrostatic pressure actually increases when a tissue becomes edematous. Ref: Barrett K.E., Barman S.M., Boitano S., Brooks H.L. (2012). Chapter 31. Blood as a Circulatory Fluid & the Dynamics of Blood & Lymph Flow. In K.E. Barrett, S.M. Barman, S. Boitano, H.L. Brooks (Eds), Ganong's Review of Medical Physiology, 24e.