Immune response to laparoscopic bowel injury.

ABSTRACT

BACKGROUND AND PURPOSE: Laparoscopic bowel injuries are rare but potentially fatal if recognition is delayed. Unlike the situation after open surgery, patients with unrecognized bowel injury after laparoscopy do not present with the typical "acute surgical abdomen." We investigated monocyte, neutrophil, and lymphocyte apoptosis as indicators of the immune response and whether this response is stimulated or suppressed by laparoscopic bowel injury compared with bowel injury induced during open surgery. MATERIALS AND METHODS: After an animal protocol was approved, laparoscopy was performed in a rabbit model. A total of 44 animals were divided into four groups of 11 rabbits each. Laparoscopic bowel injury was created using 30-W electrocautery at 0 (control), 1, and 5 hours after induction of pneumoperitoneum. Bowel injury was created in the fourth group during open laparotomy. Animals were euthanized at 0, 1 day, 1 week, or 2 weeks after surgery. Apoptosis was assessed by staining the nuclei of blood cells with H-33342 dye. RESULTS: At 1 week, neutrophil, monocyte, and lymphocyte apoptosis levels were 2.4- to 5-fold lower after laparoscopy (1-hour pneumoperitoneum) compared with open surgery. However, at 2 weeks, the percentage of apoptosis had equalized in the two groups. Interestingly, with longer laparoscopic procedures (5 hours), the percentage of apoptosis at 0 and 1 day more closely approached that seen after open surgery. At 2 weeks, there was a significant difference in apoptosis levels in all cell types between the experimental groups compared with controls (P < 0.001). No animals undergoing a 5-hour open procedure survived to 2 weeks after bowel injury. CONCLUSIONS: Open surgery resulted in a significant increase in programmed cell death compared with controls in the immediate postoperative period following bowel injury. Laparoscopic surgery produced a delayed response and after 2 weeks with bowel perforation approached open surgery levels. The difference in the degree of cellular death may be secondary to a smaller degree of stimulation of the immune response in laparoscopic surgery.