Abdominal wall sinus due to impacting gallstone during laparoscopic cholecystectomy: an unusual complication.

During laparoscopic cholecystectomy, perforation of the gallbladder can occurs in < or = 20% of cases, while gallstone spillage occurs in < or = 6% of cases. In most cases, there are no consequences. Gallstones can be lost in the abdominal wall as well as the abdomen during extraction of the gallbladder. The fate of such lost gallstones, which can lead to the formation of an abscess, an abdominal wall mass, or a persistent sinus, has not been studied adequately. Herein we report the case of a persistent sinus of the abdominal wall after an emergent laparoscopic cholecystectomy in an 82-year-old woman with gangrenous cholecystitis and perforation of the friable wall in association with an empyema of the gallbladder. The culture of the obtained pus was positive for Escherichia coli. After a small leak of dirty fluid from the wound of the epigastric port site of 4 months' duration, surgical exploration under local anesthesia revealed that the sinus was caused by spilled gallstones impacting into the abdominal wall between the posterior sheath and left rectus abdominalis muscle. The removal of the stones resulted in complete healing. Long-term complications after laparoscopic cholecystectomy involving the abdominal wall are rare but important possible consequences that could be avoided.

Helicobacter pylori infection in patients undergoing appendectomy.

AIMS: Helicobacter pylori has been found in the upper gastrointestinal tract; it is incriminated as aetiological factor in various pathological conditions. This prospective study assesses the presence of this microorganism in the appendix flora and the possible role of its infection in the pathogenesis of acute appendicitis. METHODS: H. pylori was investigated in 46 consecutive patients undergoing emergent appendectomy for presumed acute appendicitis. Blood sample for serological test of H. pylori infection was drawn before operation. The removed appendix specimen was stained for H. pylori; confirmation was made by PCR (Polymerase Chain Reaction) analysis. The intensity of inflammation was determined pathologically grading from no inflammation to gangrenous appendicitis. Statistical analysis was made using the chi-square test. RESULTS: Seropositivity for H. pylori infection was found in 18 patients (39%), but the microbe was detected in just two appendix specimens (4%). In all seropositive patients acute appendicitis was confirmed by the pathology study; serous (33%) and purulent or gangrenous (67%). The latter incidence in the seronegative patients was 50%. There were found eight specimens (17%) negative for inflammation dealing all with seronegative patients. CONCLUSIONS: It seems that H. pylori colonizes the appendix in small proportion and is unlikely to be associated in direct correlation with acute appendicitis. However, seropositive patients with acute inflammation are likely to suffer from purulent or gangrenous form.