Key words: Port site tumor recurrence — Port wound tumors — Pneumoperitoneum — Laparoscopy — Splenic tumor model — Cancer
Springer Online Journal Archives 1860-2000
Abstract Background: The etiology of port site tumor recurrences following laparoscopic surgery for cancer remains unknown. A recent study from our laboratory using a murine splenic tumor model suggests that it is poor surgical technique (i.e., crushing of the tumor) rather than the CO2 pneumoperitoneum that is responsible for these tumors. However, in that experiment, no intraabdominal procedure was carried out. We subsequently performed a preliminary study in which we compared the rate of port site tumor recurrences after laparoscopic-assisted splenectomy (LAS) vs open splenectomy (OS) using the murine splenic tumor model. In this study, we found significantly more port and incisional tumors after laparoscopic splenectomy. The reasons for this finding are unclear. Further analysis of the data showed that the incidence of port tumors in the LAS group decreased dramatically from the first to the second trial, suggesting that the experience of the surgeon may play a role. The purpose of the current study was to carry out further trials to determine if the lower rate of port tumor recurrence in the laparoscopic group will persist with increased surgical experience. Methods: Splenic tumors were established in female Balb/C mice (n= 128) via a subcapsular injection of a 0.1-cc suspension containing 105 C-26 colon adenocarcinoma cells via a left flank incision at the initial procedure. Seven days later, the animals with isolated splenic tumors (95%) were randomized to one of two groups—open splenectomy (OS) or laparoscopic-assisted splenectomy (LAS). Three ports were placed in similar locations in all animals. The OS mice underwent an open splenectomy via a subcostal incision and anesthesia for 20 min. The LAS mice underwent laparoscopic mobilization of the spleen using a three-port technique, followed by an extracorporeal splenectomy via a subcostal incision. Seven days after splenectomy, the mice were killed and inspected for abdominal wall tumor implants. The experiment was carried out in four separate trials. Results: When the results of the four trials were combined, there was no significant difference in the incidence of animals with at least one port tumor recurrence between the OS vs the LAS group (25% vs 35.2%; p= 0.30, power = 0.91). However, the overall incidence of port site tumors (number of ports with tumors/total number of ports for each group) was significantly higher in the laparoscopic-assisted group than in the open group (18.5% vs 9.5%; p= 0.03). It was noted that the incidence of port tumor recurrence (PTR) in the LAS group dropped significantly from the first to the latter three trials (second, third, and fourth trials combined) (36.1% vs 13.5%; p 〈 0.006) while it did not change significantly in the OS group. In the latter three trials, there was no significant difference in the number of animals with PTR between the LAS and the OS group (13.5% vs 9.8%; p= 0.43). Conclusions: Overall, there was no significant difference between the OS and the LAS groups in number of animals with port tumor recurrence or subcostal wound tumor recurrence. However, there were more port tumors in the laparoscopic-assisted group. The reasons for these findings are unclear. The laparoscopic mobilization was quite difficult; it required excessive splenic manipulation, which may have liberated tumor cells from the primary lesion and facilitated port tumor formation. With increased experience, less manipulation was required to complete the mobilization. Of note, the incidence of port tumors in the LAS group decreased significantly from the first to the subsequent three trials; therefore, it is possible that surgical technique is a factor in port tumor formation. The CO2 pneumoperitoneum may also be a factor, but this seems less likely.
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