The Addition of 4% Oxygen to the CO(2) Pneumoperitoneum Does Not Decrease Dramatically Port Site Metastases.

Author(s): Verguts J, Vergote I, Amant F, Moerman P, Koninckx P

Affiliation(s): Department of Obstetrics and Gynecology, University Hospital Gasthuisberg, Leuven, Belgium.

Publication date & source: 2008-11, J Minim Invasive Gynecol., 15(6):700-3.

Publication type:

STUDY OBJECTIVE: Port site metastases (PSM) after laparoscopic surgery for advanced-stage ovarian carcinoma are a cause of concern, but the pathophysiology is unknown. Because CO(2) pneumoperitoneum was recently demonstrated to be a cofactor in adhesion formation and tumor implantation in a laparoscopic mouse model, and because both could be prevented by the addition of 4% oxygen to the CO(2) pneumoperitoneum, we wanted to test the hypothesis that PSM could be related to tumor cell hypoxia during CO(2) pneumoperitoneum. DESIGN: A randomized controlled pilot trial to compare the incidence of PSM in women undergoing laparoscopy with a pure CO(2) pneumoperitoneum in comparison with women with CO(2) pneumoperitoneum with the addition of 4% oxygen (Canadian Task Force classification C). SETTING: University Hospital Gasthuisberg, Leuven, Belgium. PATIENTS: Since January 1, 2007, 22 consecutive women undergoing laparoscopy for suspected ovarian cancer with subsequent debulking laparotomy were included. INTERVENTIONS: Diagnostic laparoscopy with 100% CO(2) versus laparoscopy with addition of 4% oxygen. MEASUREMENTS AND MAIN RESULTS: In the control group, 9 (47%) PSM found in 19 port sites were excised. In the CO(2)+oxygen group, a similar incidence was found, that is, 8 (50%) PSM in 16 port sites. The incidence of PSM was higher in small women (p <.018) and in high-grade malignancies. The pathophysiology of PSM is unknown, but besides direct wound contamination, aerosolization of tumor cells and gas leaks have been suggested together with a causal relationship with the CO(2) pneumoperitoneum. Tumor cell hypoxia probably is not an important mechanism because PSM were not prevented by adding small amounts of oxygen to the CO(2) pneumoperitoneum. CONCLUSION: The hypothesis of tumor cell hypoxia by the CO(2) pneumoperitoneum as a mechanism for PSM could not be confirmed.