Changes in end-tidal carbon dioxide due to gastric perforation during pneumoperitoneum in the rat

Carbon dioxide is the most widely used gas to establish pneumoperitoneum during laparoscopic surgery. Gastrointestinal trauma may occur during the peritoneal insufflation or during the operative phase itself. Early diagnosis of these injuries is critical.

To assess changes in end-tidal carbon dioxide (ETCO2) following gastric perforation during pneumoperitoneum in the rat.

Wistar rats were anesthetized, tracheotomized and mechanically ventilated with fixed minute volume. Each animal underwent a 1 cm abdominal longitudinal incision. A 0.3 x 0.3 cm cross-incision of the stomach was performed in the perforation group but not in the controls (n = 10/group) and the abdomen was closed in both groups. After stabilization, CO2-induced pneumoperitoneum was established at 0, 5, 8 and 12 mmHg for 20 min periods consecutively, each followed by complete pressure relief for 5 min.

Ventilatory pressure increased in both groups when pneumoperitoneal pressure 5 mmHg was applied, but more so in the perforated stomach group (P = 0.003). ETCO2 increased in both groups during the experiment, but less so in the perforated group (P = 0.04). It then returned to near baseline values during pressure annulation in all perforated animals but only following the 0 and 5 mmHg periods in the controls.

When subjected to pneumoperitoneum, ETCO2 was lower in rats with a perforated stomach than in those with an intact stomach. An abrupt decrease in ETCO2 during laparoscopy may signal gastric perforation.