45. Impact of CO
2Pneumoperitoneum on Body Temperature and the
Integrity of the Peritoneal Lining
Carsten N. Gutt, M.D.
Christopher Heinbuch, M.D.
Parswa Ansari, M.D.
In addition to its well-known systemic side effects such as hypercarbia and acidosis, CO2pneumoperitoneum also has a number of detrimental local (i.e., intraperitoneal) effects. For example, intraabdominally, CO2pneumoperitonuem has been shown to reduce the blood flow to the liver [1]. Furthermore, CO2pneu- moperitoneum may also adversely effect the peritoneal lining itself. This chapter discusses the morphological alterations of the peritoneal monolayer caused by CO2pneumoperitoneum. The second part of the chapter discusses the body tem- perature alterations associated with CO2pneumoperitoneum.
A. Integrity of the Peritoneal Lining
During laparoscopic procedures, a working space must be created within the closed abdomen. The most commonly employed method of exposure is CO2
pneumoperitoneum wherein gas is insufflated until an intraabdominal pressure of 12–15 mmHg is obtained. The parietal peritoneum, which is distended and stretched by the pneumoperitoneum, is the interface between the high-pressure abdominal cavity and the abdominal wall and retroperitoneum. A sustained pneumoperitoneum initiates a variety of alterations in the mesothelial cells of the parietal peritoneum.
In a study that utilized a well-established animal model, during pneu- moperitoneum, no changes from normal morphology were observed. However, 1 to 2 hours after desufflation, the surface layer of cells demonstrated drastic alterations. The mesothelial cells had partially retracted and strongly bulged so that they appeared nearly spherical. The intercellular clefts, normally difficult to identify, were enlarged and clearly visible [2]. Further, the retraction of the cells also exposed large areas of the underlying basal lamina. On the other hand, the carpet of microvilli was nearly unchanged. The normal conformation of the mesothelium is restorable. Experiments have shown that 2 hours after release of the pneumoperitoneum the process of regeneration of the monolayer tissue is initiated. After 96 hours, the intercellular gaps are shrinking. In some
regions of the peritoneum, the insufflation-related alterations will have com- pletely disappeared and the confluent layer of microvilli-covered cells is restored.
The described ultrastructural changes observed after exposure to a high- pressure CO2environment are the same as those found after saline injection into the peritoneal cavity [3]. Thus, one might conclude that it is the increased pres- sure rather than the specific agent or gas that causes the described changes. The morphologic alterations in the superficial layer of the peritoneum, induced by increased intraabdominal pressure, are related to a loss of mesothelial integrity.
The exposed peritoneal basal lamina may in theory, under certain circumstances, have detrimental clinical consequences.
The parietal peritoneum functions physiologically as a barrier, with con- trolled pathways to remove fluids, particles, and cells from the peritoneal cavity.
The abdominal secretions are drained by large lymphatics located beneath the diaphragm’s mesothelial surface. This fluid is then transported to the venous system by the thoracic duct. In conditions associated with abdominal sepsis and peritonitis, the capnoperitoneum, by exposing the basal lamina, may provide intraabdominal infectious agents access to the bloodstream and the rest of the body. Such spread may result in bacteremia, endotoxemia, and, ultimately, septic shock. It should be noted that, thus far, there are no data to support this hypoth- esis; no studies have yet assessed bacteremia perioperatively following the instil- lation of bacteria into the abdominal cavity. However, several investigators have determined how well bacteria were “cleared” from the peritoneal cavity during laparoscopy.
One small animal study reported that bacterial clearance from the peritoneal cavity was decreased by CO2pneumoperitoneum [4]. In contrast, a second study, carried out in a porcine model, found that peritoneal bacterial clearance was increased by CO2pneumoperitoneum [5]. On the basis of these limited experi- mental data it is not possible to draw a conclusion. Can anything be gleaned from the human literature? Laparoscopic methods have been successfully used for appendectomy in the setting of perforation with complication rates similar to those noted after open surgery. Both retrospective and randomized controlled trials have failed to demonstrate a significant difference in abscess formation postoperatively [6–9]. Unfortunately, there is little literature regarding the use of laparoscopic methods for gastric or colonic perforation in humans. Clearly, further animal and human studies are needed to clarify this situation.
The uncovered basal lamina may also be a favorable environment for the attachment of viable liberated tumor cells in the abdomen. Several studies that utilized a tumor cell suspension model demonstrated that the introduction of malignant cells into the abdomen in the setting of CO2pneumoperitoneum leads to a higher tumor growth rate, a higher tumor load, and a lesser survival rate [10, 11]. It is important to note that other animal studies, carried out using similar tumor cell suspension models, have found that peritoneal tumors developed only at sites of peritoneal injury (trocar or laparotomy wound) and not on uninjured peritoneum [12, 13]. Thus, in these latter studies, the CO2pneumoperitoneum- related injury to intact parietal peritoneum was not associated with the devel- opment of peritoneal metastases in those uninjured areas. Finally, in the human arena, the recent published literature regarding laparoscopy and cancer reports no significant differences in the rate of wound or peritoneal metastases when
minimally invasive (done under CO2 pneumoperitoneum) and open surgical methods are compared.
In theory, from the standpoint of the integrity of the peritoneum, the use of CO2pneumoperitoneum may be problematic in the setting of peritonitis. As already noted, there are not enough human or animal data available to draw any firm conclusions. In the setting of cancer, one can raise similar concerns about CO2pneumoperitoneum increasing the chances of peritoneal tumor metastases.
However, as per the available and ever-enlarging human literature, increased rates of wound and peritoneal tumor recurrences have not been reported. Thus, presently, it appears as though the insufflation-related peritoneal alterations are not of clinical consequence.
B. Impact of Pneumoperitoneum on Body Temperature
Perioperative hypothermia increases the morbidity of surgery. Hypothermia is associated with higher rates of postoperative wound infection [14], more adverse cardiac events [15], and greater transfusion requirements [16].
Initially, it was anticipated that laparoscopic surgery would be associated with less hypothermia than open surgery because the abdomen remains closed with the former, thus avoiding prolonged exposure of the abdominal viscera to the cool room air. However, thus far, most studies have not found a difference in the rate or extent of hypothermia when open and laparoscopic procedures are compared. Luck et al. found no statistically significant difference in the incidence of hypothermia during colorectal cases when well-matched patients undergoing open and laparoscopic surgery were compared [17]. Similarly, Nguyen et al.
demonstrated a decrease in intraabdominal temperature but not core temperature when comparing laparoscopic versus open gastric bypass procedures [18].
The risk of hypothermia due to CO2insufflation during laparoscopic surgery was highlighted by Bessell et al. in 1995 [19]. The risk appears to be correlated with the duration of the operation and the insufflation flow rate. Modern elec- tronic insufflator units are able to maintain the pneumoperitoneum at a constant pressure by continuous insufflation of gas to replace losses caused by leaks and the dissolution of CO2 in the blood. This means that during a complex or advanced operation, hundreds of liters of gas may be insufflated into the abdomen.
The temperature of the gas leaving the insufflator has been shown to be about 25°C. Early after insufflation into the abdomen, the temperature of the gas is in the range of 30°–32°C. Obviously, this intraperitoneal hypothermia, relative to the core temperature, would be expected to cause a drop in the core tempera- ture. If there is minimal leakage of CO2from the abdomen, then, with time, the gas will become warmer. Unfortunately, during most advanced cases there are substantial and, at times, nearly continuous leaks such that additional cold gas must be insufflated regularly to maintain the pressure and exposure. In addition, animal studies suggest that a major contributing factor to heat loss is evapora-
tion, which can be rectified by humidifying the gas [20]. Thus, it is not surpris- ing that laparoscopic procedures, similar to open procedures (but for different reasons), are often associated with a drop in core temperature.
There is evidence that the use of heated and humidified gas lessens the pro- cedure-related hypothermia. In a single large animal study, the differences in core temperatures after cool and warm CO2insufflation were significant [19]. A recent randomized trial in humans found that patients receiving heated and humidified CO2demonstrated significantly higher intraabdominal temperatures;
of note, no differences in core temperatures were found [21]. A second human study also reported some advantages when humidified and warmed (to body temperature) CO2was utilized [22]. Other studies have found that the vasodila- tory effects of warmed CO2are not important from a thermal point of view.
Therefore, some controversy exists regarding the effectiveness and impact of warmed and humidified CO2in regard to intraperitoneal thermoregulation. Of note, the use of warm and/or humidified CO2has been noted to have other effects in addition to those relating to temperature.
One study noted that warm CO2 insufflation was associated with local vasodilatation in the kidneys; this might be beneficial to patients with border- line renal function [23]. Of uncertain significance, in another study, the use of very dry CO2was associated with increased peritoneal fluid viscosity [24]. The use of warm or humidified pneumoperitoneum has also been associated with decreased postoperative pain [25, 26]. Finally, Puttick et al. reported that warming and humidifying the insufflation gas led to a reduced postoperative intraperitoneal acute-phase cytokine response [27].
In summary, there are conflicting data regarding the impact of warmed and humidified CO2on surgery-related hypothermia; of note, postoperative pain may be reduced. There are enough encouraging reports, in the opinion of the authors, to warrant the use of gas-warming units and humidifiers, especially during lengthy cases. An effort should also be made to minimize the leakage of CO2
from the peritoneal cavity.
C. References
1. Jakimowicz J, Stultiens G, Smulders F. Laparoscopic insufflation of the abdomen reduces portal venous flow. Surg Endosc 1998;12(2):129–132.
2. Volz J, Köster S, Spacek Z, Paweletz N. Characteristic alteration of the peritoneum after carbon dioxide pneumoperitoneum. Surg Endosc 1999;13:611–614.
3. Tsilibary EC, Wissig SL. Lymphatic absorption from the peritoneal cavity: regulation of patency of mesothelial stomata. Microvasc Res 1983;25:22–29.
4. Chekan EG, Nataraj C, Clary EM, et al. The effect of gases in the intraperitoneal space on cytokine response and bacterial translocation in a rat model. Surg Endosc 1999;
13(11):1135–1138.
5. Collet D, Vitale GC, Reynolds M, Klar E, Cheadle WG. Peritoneal host defenses are less impaired by laparoscopy than by open operation. Surg Endosc 1995;9(10):
1059–1064.
6. Pedersen AG, Petersen OB, Wara P, Ronning H, Qvist N, Laurberg S. Randomized clinical trial of laparoscopic versus open appendicectomy. Br J Surg 2001;88(2):
200–205.
7. Tang E, Ortega AE, Anthone GJ, Beart RW Jr. Intraabdominal abscesses following laparoscopic and open appendectomies. Surg Endosc 1996;10(3):327–328.
8. Champault GG, Barrat C, Raselli R, Elizalde A, Catheline JM. Laparoscopic versus open surgery for colorectal carcinoma: a prospective clinical trial involving 157 cases with a mean follow-up of 5 years. Surg Laparosc Endosc Percutan Tech 2002;12(2):
88–95.
9. Wullstein C, Barkhausen S, Gross E. Results of laparoscopic vs. conventional appen- dectomy in complicated appendicitis. Dis Colon Rectum 2001;44(11):1700–1705.
10. Volz J, Köster S, Leweling H, Melchert F. Surgical trauma and metabolic changes induced by surgical laparoscopy vs. laparotomy. Gynecol Endosc 1997;6:1–6.
11. Volz J, Köster S, Schaef B, Paolucci V. Laparoscopic surgery: the effects of insuf- flation gas on tumor-induced lethality in mice. Am J Obstet Gynecol 1998;174:132–
140.
12. Jones DB, Guo LW, Reinhard MK, et al. Impact of pneumoperitoneum on trocar site implantation of colon cancer in hamster model. Dis Colon Rectum 1995;38:1182–
1188.
13. Wu JS, Brasfield EB, Guo LW, et al. Implantation of colon cancer at trocar sites is increased by low pressure pneumoperitoneum. Surgery 1997;122(1):1–7.
14. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and reduce hospitalisation. N Engl J Med 1996;334:
1209–1215.
15. Jones HD, McLaren CAR. Perioperative shivering and hypoxaemia after halothane, nitrous oxide, and oxygen anaesthesia. Br J Anaesth 1965;37:35–41.
16. Schmeid H, Kurz A, Sessler DI, Kozek Z, Reiter A. Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty. Lancet 1996;347:
289–292.
17. Luck AJ, Moyes D, Maddern GJ, Hewett PJ. Core temperature changes during open laparoscopic colorectal surgery. Surg Endosc 1999;13:480–483.
18. Nguyen NT, Fleming NW, Singh A, Lee SJ, Goldman CD, Wolfe BM. Evaluation of core temperature during laparoscopic and open gastric bypass. Obes Surg 2001;11(5):
570–575.
19. Bessell JR, Karatassas A, Patterson JR, Jamieson GG, Maddern GJ. Hypothermia induced by laparoscopic insufflation: a randomised study in a pig model. Surg Endosc 1995;9:791–796.
20. Bessell JR, Ludbrook G, Millard SH, Baxter PS, Ubhi SS, Maddern GJ. Humidified gas prevents hypothermia induced by laparoscopic insufflation: a randomized con- trolled study in a pig model. Surg Endosc 1999;13(2):101–105.
21. Nguyen NT, Furdui G, Fleming NW, et al. Effect of heated and humidified carbon dioxide gas on core temperature and postoperative pain: a randomized trial. Surg Endosc 2002;16(7):1050–1054.
22. Ott DE, Reich H, Love B, et al. Reduction of laparoscopic-induced hypothermia, post- operative pain and recovery room length of stay by pre-conditioning gas with the Insu-
flow device: a prospective randomized controlled multi-center study. J Soc Laparosc Surg 1998;2(4):321–329.
23. Bäcklund M, Kellokumpu I, Scheinin T, von Schmitten, Tikkanen I, Lindgren L. Effect of temperature of insufflated CO2during and after prolonged laparoscopic surgery.
Surg Endosc 1998;12:1126–1130.
24. Ott DE. Laparoscopic and tribology: the effect of laparoscopic gas on peritoneal fluid.
J Am Assoc Gynecol Laparosc 2001;8:117–123.
25. Mouton WG, Bessell JR, Millard SH, Baxter PS, Maddern GJ. A randomized con- trolled trial assessing the benefit of humidified insufflation gas during laparoscopic surgery. Surg Endosc 1999;13(2):106–108.
26. Mouton WG, Bessell JR, Otten KT, Maddern GJ. Pain after laparoscopy. Surg Endosc 1999;13:445–448.
27. Puttick MI, Scott-Coombes DM, Dye J, et al. Comparison of immunologic and phys- iologic effects of CO2 pneumoperitoneum at room and body temperatures. Surg Endosc 1999;13:572–575.
