Effect of Small Bowel Perforation During Laparoscopy on End-Tidal Carbon Dioxide: Observation in a Small Animal Model

IntroductionThere are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO2) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO2 in a rat model.Materials and methodsTwo groups of Wistar rats (n = 8/group) were anesthetized, tracheostomized, and mechanically ventilated at a fixed tidal volume and respiratory rate. After a stabilization phase of 30 min, CO2 pneumoperitoneum was established to 5 mmHg in one group and 12 mmHg in the other group, and maintained for 30 min. A small bowel perforation was then created and pneumoperitoneum was reestablished for another 30 min. Blood pressure, heart rate, peak ventilatory pressure, and ETCO2 were recorded throughout the experiment.ResultsNo significant changes in blood pressure throughout the experiment were noted in either group. The ventilatory pressure increased in both groups after the induction of pneumoperitoneum. In the 5 mmHg group, there was a modest increase in ETCO2 following the induction of pneumoperitoneum (from 39.4 ± 1.9 to 41.1 ± 1.4, P = 0.014), and a further increase following the small bowel perforation (from 41.1 ± 1.4 to 42 ± 0.8, P = 0.007). In the 12 mmHg group, there was no change in ETCO2 after the induction of pneumoperitoneum; however, there was a substantial increase in ETCO2 following bowel perforation (35.0 ± 2.0 to 49.8 ± 7.1, P = 0.002).ConclusionsETCO2 increases when the small bowel is perforated during CO2 pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO2 through the bowel mucosa, causing ETCO2 elevation. Therefore, an abrupt increase in ETCO2 observed during laparoscopy may indicate small bowel injury.