TY - JOUR
T1 - The Addition of 4% Oxygen to the CO2 Pneumoperitoneum Does Not Decrease Dramatically Port Site Metastases
AU - Verguts, Jasper
AU - Vergote, Ignace
AU - Amant, Frederic
AU - Moerman, Philippe
AU - Koninckx, Philippe
PY - 2008
Y1 - 2008
N2 - 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 CO2 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 CO2 pneumoperitoneum, we wanted to test the hypothesis that PSM could be related to tumor cell hypoxia during CO, pneumoperitoneum. Design: A randomized controlled pilot trial to compare the incidence of PSM in women undergoing laparoscopy with a pure CO2 pneumoperitoneum in comparison with women With CO2 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% CO2 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 CO2+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 CO2 pneumoperitoneum. Tumor cell hypoxia probably is not an important mechanism because PSM were not prevented by adding small amounts of oxygen to the CO2 pneumoperitoneum. Conclusion: The hypothesis of tumor cell hypoxia by the CO2 pneumoperitoneum as a mechanism for PSM could not be confirmed. Journal of Minimally Invasive Gynecology (2008) 15, 700-703 (C) 2008 AAGL. All rights reserved
AB - 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 CO2 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 CO2 pneumoperitoneum, we wanted to test the hypothesis that PSM could be related to tumor cell hypoxia during CO, pneumoperitoneum. Design: A randomized controlled pilot trial to compare the incidence of PSM in women undergoing laparoscopy with a pure CO2 pneumoperitoneum in comparison with women With CO2 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% CO2 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 CO2+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 CO2 pneumoperitoneum. Tumor cell hypoxia probably is not an important mechanism because PSM were not prevented by adding small amounts of oxygen to the CO2 pneumoperitoneum. Conclusion: The hypothesis of tumor cell hypoxia by the CO2 pneumoperitoneum as a mechanism for PSM could not be confirmed. Journal of Minimally Invasive Gynecology (2008) 15, 700-703 (C) 2008 AAGL. All rights reserved
U2 - https://doi.org/10.1016/j.jmig.2008.07.021
DO - https://doi.org/10.1016/j.jmig.2008.07.021
M3 - Article
C2 - 18971132
SN - 1553-4650
VL - 15
SP - 700
EP - 703
JO - Journal of Minimally Invasive Gynecology
JF - Journal of Minimally Invasive Gynecology
IS - 6
ER -