Pneumoperitoneum and peritoneal surface changes A review S. J. Neuhaus, D. I. Watson Flinders University Department of Surgery, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia Received: 28 July 2003/Accepted: 7 January 2004/Online publication: 12 May 2004 Abstract Background: Recent evidence suggests that the use of carbon dioxide to create a pneumoperitoneum during laparoscopy can lead to adverse structural, metabolic, and immune derangements within the peritoneal cavity, and that these can be dependent on the specific insuf- flation gas used. These changes include structural alterations in the mesothelial lining, pH disturbances, and alterations in peritoneal macrophage responsive- ness. This contrasts with an apparent systemic benefit associated with laparoscopic, as compared with open, surgery. Methods: Recently published clinical and experimental studies related to the effect of pneumoperitoneum on the peritoneal surface are reviewed, and their relevance is discussed. Results: Structural changes in the peritoneal mesothelial surface layer such as widening of the intercellular junc- tions can be demonstrated with electron microscopy. Acidification of the peritoneum in response to carbon dioxide insufflation occurs not only at the peritoneal surface, but also in the underlying connective tissue, resulting in disturbances in the electrical surface charge and the release of various immune mediators such as endotoxin. Pneumoperitoneum also affects the local peritoneal immune environment resulting in alterations in cytokine production and phagocytic function, as well as diminished antitumor cell cytotoxicity. Conclusions: Ultrastructural, metabolic, and immune alterations are observed at the peritoneal surface in re- sponse to a pneumoperitoneum. Experimental evidence suggests that these changes are carbon dioxide–specific effects. The consequences of these alterations to the local peritoneal environment are not well understood, but they may facilitate tumor implantation within the peri- toneal cavity and adversely affect the ability to clear intraperitoneal infections. Further investigation into this area is warranted. Key words: Laparoscopy pneumoperitoneum Insufflation gasses — Carbon dioxide peritoneum Recent evidence suggests that the use of carbon dioxide (CO 2 ) to create a pneumoperitoneum during laparos- copy does not simply create a working space for sur- gery, but can lead to adverse structural, metabolic, and immune derangements within the peritoneal cavity, and that these can be dependent on the specific insufflation gas used. These changes include structural alterations in the mesothelial lining, pH disturbances, and altera- tions in peritoneal macrophage responsiveness. Fur- thermore, these effects might be clinically important, and they have been invoked as a possible explanation for the potential problem of port-site metastases after laparoscopic cancer surgery. To examine this issue further, we reviewed recently published literature describing the outcomes of clinical and experimental studies that investigated the effect of laparoscopic insufflation on the peritoneum. To do this we used PubMed to search for relevant articles published since 1985. Additional references were sourced from the reference lists in some of these articles. The peritoneal structural environment The peritoneum comprises a single continuous layer of mesothelial cells 2.5 to 3lm thick and covered with microvilli [51]. These cells, joined by tight junctions and desmosomes, rest on a basement membrane, below which is a layer of fibrous connective tissue. The creation of a pneumoperitoneum has been shown to cause struc- tural changes in the peritoneal mesothelial surface layer, which are visible microscopically [48]. This could be attributable to the use of CO 2 per se, or it might be attributable to desiccation of the peritoneal surface by cold insufflation gas (independently of the gas type). Correspondence to: D. I. Watson Surg Endosc (2004) 18: 1316–1322 DOI: 10.1007/s00464-003-8238-2 Ó Springer Science+Business Media, Inc. 2004