Sw. Lee et al., TRAUMATIC HANDLING OF THE TUMOR INDEPENDENT OF PNEUMOPERITONEUM INCREASES PORT SITE IMPLANTATION RATE OF COLON-CANCER IN A MURINE MODEL, Surgical endoscopy, 12(6), 1998, pp. 828-834
Background: Reports of port site tumor recurrences after laparoscopic-
assisted resection of colon tumors have raised concerns about the safe
ty of laparoscopic cancer surgery. Tumor cell suspension studies in an
imals have implicated the CO2 pneumoperitoneum (pneumo) in the etiolog
y of port tumors. Unfortunately, in several ways, the cell suspension
model is unrealistic and does not permit assessment of how tumor cells
become liberated from the primary tumor. The purpose of this study wa
s to establish a more realistic splenic tumor model and to determine t
he relative importance of the CO2 pneumo and excessive surgical manipu
lation in the development of port site and incisional tumor recurrence
s.Methods: Splenic tumors were established in female Balb/C mice (n =
134) via a subcapsular injection of 10(5) C-26 colon adenocarcinoma ce
lls (0.1 ml volume) via a left-flank incision at the initial procedure
. Ten days later, the animals were reexplored via a 1-cm left subcosta
l incision. Those with isolated splenic tumors (95%) were randomized i
nto one of four groups: (a) control, (b) CO2 pneumo, (c) crushed tumor
, or (d) crushed tumor with pneumo. Ports were placed in the left lowe
r, light lower, and right upper quadrants of each mouse. In groups 1 a
nd 2, the mice underwent a meticulously performed splenectomy; in grou
ps 3 and 4, the tumor capsule was crushed intraabdominally prior to sp
lenectomy. In groups 1 and 3, the subcostal incision was closed and th
e ports were removed after 15 min of anesthesia. Following splenectomy
, group 2 and group 4 mice underwent closure of the subcostal incision
and a 15-min CO2 pneumo (4-6 mm Hg) after which the ports were remove
d. Twelve days later, the mice were killed and examined for abdominal
wall tumor implants. Results: Significantly more animals in group 3 (c
rushed tumor) developed port site and incisional tumors than those in
group 1 (control) (p < 0.002 for both comparisons). The same results w
ere found when group 4 (crush plus pneumo) was compared to group 2 (pn
eumo) (p < 0.002 for both comparisons). Regarding the port wounds, whe
n the ports are considered individually (number of ports with tumors/t
otal number of ports for each group), there were significantly more po
rt tumors in the two crush groups than in the noncrush groups. No sign
ificant differences were noted when the port site and incisional tumor
rates for group (control) and group 2 (pneumo) were compared or when
the results for group 2 (crush) and group 4 (crush pneumo) were compar
ed. Conclusions: A splenic tumor model was successfully established. W
hen compared to meticulous technique, pur posefully traumatic handling
of the splenic tumor before resection resulted in significantly more
port wound and incisional tumors. In contrast, the addition of a pneum
o after splenectomy did not significantly influence the incidence of p
ort tumors in either the ''good'' or the ''poor'' technique groups. Th
ese results suggest that surgical technique plays a larger role in the
development of port site tumors than the CO2 pneumoperitoneum.