The role of peritoneal immunity and the tumour-bearing state on the development of wound and peritoneal metastases after laparoscopy

Background: The effect of the tumour-hearing state and alterations in peritoneal immune function on the incidence of port-site and peritoneal metastases was investigated after laparoscopy with and without CO2 pneumoperitoneum. Methods: A suspension of viable adenocarcinoma cells was introduced into the left upper quadrant of the peritoneal cavity of syngeneic tumour-bearing rats at laparotomy, laparoscopy with CO2, and gasless laparoscopy. Control mts did not have pre-existing rumours. A group of non-tumour-bearing rats were also injected intraperitoneally with endotoxin I h before intraperitoneal tumour cell injection. Six days later the peritoneal cavity and surgical wounds were examined for macroscopic evidence of implanted tumour. Peritoneal macrophages were obtained from tumour-hearing rats subjected to different laparoscopic procedures and the activation state measured following exposure to lipopolysaccharide in vitro. Results: In the control rats, tumour implantation in the surgical wounds and peritoneum was significantly greater in the rats that had undergone laparoscopy with CO2. The presence of a pre-existing tumour was associated with increased tumour spread in all treatment groups and at most sites. Injection of endotoxin also resulted in increased tumour spread. Peritoneal macrophages from control and tumour-bearing rats who underwent laparoscopy with CO2 produced significantly less TNF-alpha in vitro, compared to gasless laparoscopy or laparotomy. Conclusions: Carbon dioxide insufflation enhances tumour spread and implantation The underlying immune or metabolic status of the host, as influenced by the tumour-hearing state or modification of the peritoneal environment, also has a marked independent effect on tumour spread and implantation The immune and metabolic status of the peritoneum including the extent of macrophage activation is implicated in this effect.