ABSTRACT
In 1931, Sampson described the peritoneal dissemination of ovarian cancer as follows: (1) escape of the cancer cells from the primary ovarian tumor into the free peritoneal cavity; (2) migration of these cells to their site of implantation; (3) reaction of the peritoneal surface injured by the cancer cells so that fibrin and organization of this fibrin occur; and (4) progression of the cancerous implant at that site.1 The clockwise motion of the peritoneal fluid in the abdominal cavity, driven by intestinal peristalsis and diaphragmatic excursion during respiration, accounts for the characteristic distribution pattern of ovarian cancer. Exfoliated tumor cells have a tendency to implant on fixed structures and in areas where resorption of peritoneal fluid occurs, such as the under-surfaces of the diaphragms and omentum. These cells tend to follow the circulatory path of the peritoneal fluid and implant along the surfaces of the peritoneal cavity, especially those of the intestines and their mesenteries as well as the omentum.
