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Effects of adding small amounts of oxygen to a carbon dioxide-pneumoperitoneum of increasing pressure in rabbit ventilation models
Abstract
To evaluate the metabolic consequences of the addition of oxygen to the CO(2)-pneumoperitoneum.
Prospective randomized study in rabbits. After 30 minutes of ventilation pneumoperitoneum was maintained for 90 minutes with pure CO(2) or CO(2) with 2% or 6% of oxygen. The intraperitoneal pressure was increased from 10 to 15 and 20 mm Hg every 30 minutes. Ventilation rate was either fixed or a progressive hyperventilation. End points were changes in arterial blood gases (Pco(2), Po(2)), pH, acid-base balance (actual base excess [ABE], standard bicarbonate [SBC], standard base excess [SBE], hydrogen carbonate [HCO(3)(-)], concentration of total carbon dioxide [Tco(2)]); oxygen and oximetry (oxyhemoglobin [O(2)Hb], oxygen saturation [So(2)], reduced hemoglobin [RHb], total oxygen concentration [To(2)], and oxygen tension at half saturation assessing hemoglobin oxygen affinity [p50]); and lactate concentrations assayed every 15 minutes.
University research center.
Twenty-four adult female New Zealand white rabbits.
Anesthesia, mechanical ventilation, and pneumoperitoneum.
The effects of CO(2)-pneumoperitoneum on all end points increased with the elevated intraperitoneal pressure and were more pronounced when ventilation was fixed. Changes were less when 2% or 6% of oxygen had been added to the CO(2)-pneumoperitoneum. With use of logistic regression, the addition of oxygen, intraperitoneal pressure, and ventilation were found to be independent variables affecting Pco(2), pH, ABE, SBE, HCO(3)(-), O(2)Hb, So(2), p50, and end-tidal CO(2).
The metabolic consequences of the combined effect of increased intraperitoneal pressure and CO(2)-pneumoperitoneum were less when 2% to 6% of oxygen was added or when animals were hyperventilated. We suggest that metabolic and mesothelial hypoxemia caused by CO(2) absorption can be reduced by adding small amounts of oxygen and by hyperventilation.
... The authors clearly demonstrated significant changes of the peak in respiratory pressure, dynamic lung compliance, P ET CO 2 , arterial pO 2 , pCO 2 , and pH values at the 30th min of CO 2 -pneumoperitoneum in comparison with parameters of both at the baseline and at the end of surgery. These changes we considered as consequences of a causative force of CO 2 -insufflation with increased content of CO 2 in the body (rise of P ET CO 2 and arterial pCO 2 ), with subsequent mild respiratory or severe acidosis (reduced pH) depending on intraperitoneal pressure rate and CO 2 -pneumoperitoneum duration [4][5][6]. Subsequently, the dynamic lung compliance was reduced with increased peak of respiratory pressure in adult patients with ASA I/II [1]. ...
We read with great interest the recently published article by Davarcı et al. [1] in your journal aimed at studying the effects of CO2-pneumoperitoneum at 12 mm Hg intraperitoneal pressure on end-tidal CO2 (CO2) concentration, arterial blood gas values and oxidative stress markers in blood, and bronchial lavage during laparoscopic cholecystectomy using a long protective strategy since our clinical [2] and experimental [3] results were in line with findings of this study [1]. The authors clearly demonstrated significant changes of the peak in respiratory pressure, dynamic lung compliance, CO2, arterial pO2, pCO2, and pH values at the 30th min of CO2-pneumoperitoneum in comparison with parameters of both at the baseline and at the end of surgery. These changes we considered as consequences of a causative force of CO2-insufflation with increased content of CO2 in the body (rise of CO2 and arterial pCO2), with subsequent mild respiratory or severe acidosis (reduced pH) depending on intraperitoneal pressure rate and CO2-pneumoperitoneum duration [4–6]. Subsequently, the dynamic lung compliance was reduced with increased peak of respiratory pressure in adult patients with ASA I/II [1].
We have monitored respiratory and cardiovascular parameters (systolic/diastolic arterial pressure, heart rate, cardiac output, ventilation rate and pressure, tidal volume, and CO2), the dynamic lung compliance, the peak in respiratory pressure, skin temperature, and urine output with catheter in 12 newborns suffering laparoscopic surgical procedures due to ovarian tumors [2]. All samples were collected at the time of induction, at the time of incision, and every 10 minutes during surgery and after surgery during one and a half hours, subsequently at the eleven time points (0–10). All babies were born at the full term pregnancies with body weight above 3000 g. Anesthesia was induced by Relanium or Midazolam (0,63 ± 0,27 mg/kg/h) and Fentanyl (11,9 ± 5,8 μg/kg/h); pressure controlled mechanical ventilation was done by means of anesthesia-respiratory ventilator (Drager) supplemented with myorelaxants (cisatracurium besilate 0,14 ± 0,05 mg/kg/h or Atracurium 0,54 ± 0,19 mg/kg/h).
In newborns during laparoscopic surgery, CO2 value was significantly increased (Figure 1(a)) during the first 20 minutes of CO2-pneumoperitoneum at the 7–9 mm Hg of intraperitoneal pressure, which was corrected by mild hyperventilation with increased ventilation rate (VR). These changes were accompanied with increased systolic and diastolic arterial blood pressure and decreased cardiac output [2]. Moreover, such parameters as respiratory volume, minute ventilation rate, and dynamic lung compliance were reduced with increased peak of respiratory pressure, whereas heart rate, urine output, and skin temperature were remaining stable [2].
... We previously demonstrated that reduced blood gas changes during CO 2 pneumoperitoneum are associated with mixed gas insufflation (MGI) since even a small concentration of O 2 added to CO 2 results in lower end tidal CO 2 (P ET CO 2 ) values and slight changes in blood gas parameters in comparison with those of pure CO 2 insufflation in rabbits [2,3]. Also, MGI has a significant impact on ventilation parameters [4]. ...
No abstract available.
... However, laparoscopic surgery entails other, specific effects due to the use of gas media to extend the abdomen . From this, a large body of literature has sprung studying the pathophysiologic mechanisms of CO 2 pneumoperitoneum induced systemic alterations such as respiratory, cardiovascular and blood gas, acid base parameters changes, as well as local disturbances in the peritoneal cavity such as decreased peritoneal pH and blood circulatory deteriorations with mesothelial hypoxemia during laparoscopic surgery242526272829 . The discussion has polarised: some claim these changes have a crucial impact on postsurgical complications such as adhesion formation and port-site cancer metastasis3031323334 others say these changes have no or little impact on postsurgical complications [16,17,28,29]. ...
Many factors have been put forward as a driving mechanism of surgery-triggered adhesion formation (AF). In this study, we underline the key role of specific surgical trauma related with open surgery (OS) and laparoscopic (LS) conditions in postoperative AF and we aimed to study peritoneal tissue inflammatory reaction (TIR), remodelling specific complications of open surgery (OS) versus LS and subsequently evaluating AF induced by these conditions.
A prospective randomized study was done in 80 anaesthetised female Wistar rats divided equally into 2 groups. Specific traumatic OS conditions were induced by midline incision line (MIL) extension and tissue drying and specific LS conditions were remodelled by intraperitoneal CO2 insufflation at the 10 cm of water. TIR was evaluated at the 24th, 72nd, 120th and 168th hour by scoring scale. Statistical analysis was performed by the non-parametric t test and two-way ANOVA using Bonferroni post-tests.
More pronounced residual TIR was registered after OS than after LS. There were no significant TIR interactions though highly significant differences were observed between the OS and LS groups (p < 0.0001) with regard to surgical and time factors. The TIR change differences between the OS and LS groups were pronounced with postoperative time p < 0.05 at the 24th and 72nd; p < 0.01--120th and p < 0.001--168th hrs. Adhesion free wounds were observed in 20.0 and 31.0% of cases after creation of OS and LS conditions respectively; with no significant differences between these values (p > 0.05). However larger adhesion size (41.67 ± 33.63) was observed after OS in comparison with LS (20.31 ± 16.38). The upper-lower 95% confidential limits ranged from 60.29 to 23.04 and from 29.04 to 11.59 respectively after OS and LS groups with significant differences (p = 0.03). Analogous changes were observed in adhesion severity values. Subsequently, severe TIR parameters were followed by larger sizes of severe postoperative adhesions in the OS group than those observed in the LS group.
MIL extension and tissue drying seem to be the key factors in the pathogenesis of adhesion formation, triggering severe inflammatory reactions of the peritoneal tissue surrounding the MIL resulting in local and systemic consequences. CO2 insufflation however, led to moderate inflammation and less adhesion formation.
Objectives: The aims of this study were to analyze the specific risk factors during the treatment of metabolic diseases when using laparoscopic Roux-en-Y gastric bypass (LRYGB), and to explore and identify a system for intraoperative nursing problems and the effects of corresponding nursing interventions. Methods: A systems for intraoperative nursing problems was established by taking 44 patients who underwent LRYGB from May 2010 to November 2012 at the First Affiliated Hospital of Wenzhou Medical University. The constituent ratio of the specific risk factors and nursing problems and the effects of the corresponding nursing interventions for specific risk factors were analyzed. Results: The specific intraoperative nursing problems of LRYGB found include risk for aspiration and deficient fluid volume, hypothermia, suffocation, tissue hypoperfusion, and diabetic ketoacidosis (DKA), which correlated with age (p<0.05). After appropriate nursing interventions, risks for suffocation, aspiration, DKA, and hypothermia were significantly reduced (p<0.05). Conclusions: Identifying nursing problems during LRYGB may provide guidance for the intraoperative nursing team. Understanding the corresponding nursing interventions can reduce the incidence rate of potential risks, and hence improve the safety of the procedure.
A prospective randomized trial in a rabbit model was performed to test the hypothesis that the increase in adhesion formation following prolonged pneumoperitoneum is mediated by peritoneal hypoxaemia. Laparoscopic standardized opposing lesions were performed in uterine horns and pelvic sidewalls by bipolar coagulation and CO(2) laser in six groups of eight animals. Pure CO(2) or helium pneumoperitoneum was used for 10 (groups I and IV) or 45 min (groups II and V) to confirm the effect of duration of pneumoperitoneum and 96% of CO(2) or helium with 4% of oxygen (group III and VI) for 45 min to assess the effect of the addition of oxygen. After 7 days, adhesion formation was scored by laparoscopy. By two-way analysis of variance, total, extent, type and tenacity of adhesion scores increased (P = 0.0003, P = 0.0004, P = 0.0004 and P = 0.004) with increasing duration of pneumoperitoneum and decreased (P = 0.02, P = 0.03, P = 0.01 and P = 0.05) with the addition of oxygen. No differences were found between CO(2) and helium. In conclusion these data confirm the effect of pneumoperitoneum upon adhesions and demonstrate its reduction by oxygen, strongly suggesting that the main cause of adhesion formation is the relatively superficial hypoxaemia produced by the pneumoperitoneum.
CO(2)-pneumoperitoneum used in endoscopic surgery induces system effects by CO(2) absorption. This study investigated the effect of the addition of O(2) to CO(2)-pneumoperitoneum, upon CO(2) absorption.
The effect of a pneumoperitoneum using 100% CO(2) or 94% CO(2) + 6% O(2) upon arterial blood gases, acid base and O(2) homeostasis was evaluated. In series A suboptimal ventilation and a pneumoperitoneum pressure (PP) of 10 mmHg was used. In series B adequate ventilation and PP of 6 mmHg was used.
CO(2)-pneumoperitoneum profoundly affected blood gases and acid base homeostasis i.e. increasing pCO(2), HCO(3)(P < 0.001) and lactate concentrations (P < 0.05) and decreasing pH, actual base excess and standard bicarbonate (P < 0.001), resulting in metabolic hypoxaemia with desaturation, lower pO(2) (P < 0.001) and O(2)Hb (P < 0.05). These effects were more pronounced with higher PP and suboptimal ventilation.
CO(2)-pneumoperitoneum profoundly affected blood gases and acid base homeostasis resulting in metabolic hypoxaemia. The addition of 6% of O(2) to the CO(2)-pneumoperitoneum prevented these effects to a large extent. If these preliminary data are confirmed in the human, the addition of a few percent of O(2) to CO(2) could become important for endoscopic surgery of long duration, especially in obese patients with limited cardiorespiratory adaptation and steep Trendelenburg.
Post-operative adhesion formation is a major clinical problem. Tissue oxygenation is one of the most important determinants in adhesion formation. The objective of this study was to investigate whether supplemental perioperative oxygen could reduce post-operative adhesion formation through increasing the peritoneal tissue oxygen tension (PitO(2)) in a mouse model.
Adult C57BJ6 mice were randomly assigned to two groups: Group 1 (n = 20), Fraction of Inspired Oxygen (FiO(2)): 0.21; Group 2 (n = 20), FiO(2): 0.80. On day 0, over the course of the 90 min procedure including the 60 min of laparotomy, PitO(2) was continuously monitored. On day 7, a second laparotomy was performed to assess abdominal wound adhesions. Real-time RT-PCR was performed to measure expression levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) mRNA in peritoneal tissues.
The PitO(2) levels in Group 2 were significantly higher compared to Group 1 (P < 0.001) and controls (P < 0.003). There was no significant difference in the incidence of abdominal wound adhesions; however, the severity of adhesions was significantly reduced in Group 2 compared to Group 1 (P < 0.03). A significantly higher tPA/PAI-1 mRNA ratio was detected in Group 2 and the controls compared to Group 1 (P < 0.02 and P < 0.002, respectively).
Supplemental perioperative oxygen may help to reduce post-operative adhesion formation.
Study Objective. To identify oxidative stress in peritoneum during laparoscopic and open surgery by measuring products of lipid peroxidation, and to determine whether surgical approach influences the type of oxidative metabolite synthesized. Design. Retrospective analysis (Canadian Task Force classification II-2). Setting. University-affiliated hospital. Patients. Twenty-eight consecutive women with uterine myomas or ovarian cysts. Intervention. Laparoscopic or open surgery (14 patients each). Measurements and Main Results. We obtained 1 x 1-cm squares of peritoneum at the beginning and end of surgical procedures away from sites of surgery. 8-Isoprostaglandin F-2alpha, hydroxyeicosatetranoic acids (HETEs), and malondyaldehyde (MDA) were measured by enzyme-immunoassay, high-performance liquid chromatography, and thiobarbituric acid adduction method, respectively. Comparisons showed significant increases in 5-HETE and 8-prostane in the laparoscopy group, which were correlated with duration of pneumoperitoneum and volume of carbon dioxide (CO2) insufflated, respectively. In the laparotomy group only MDA rose significantly related to duration of surgery. Conclusion. Lipid peroxidation was observed in peripheral peritoneum during laparoscopic surgery, mediated through noncyclooxygenase and lipoxygenase pathways, and appears to be due to effects of CO2 pneumoperitoneum. Biochemical reactions were also observed in the laparotomy group, but are thought to be related to mechanisms other than lipid peroxidation.
With improvement in technology and growing surgical expertise, more extensive and prolonged laparoscopic procedures will be
performed in a wide range of patients. Modification of the anesthetic technique and the prevention of common postoperative
complications including pain, nausea, and vomiting using the multimodal approach should allow early recovery. Although the
laparoscopic approach provides significant benefits, a thorough understanding of the associated cardiopulmonary changes and
the potential complications is necessary to maintain patient safety.
Study objective:
To investigate the effects of peritoneal exposure to carbon dioxide (CO2) on peritoneal microcirculation and free radical scavenger (FRS) metabolism, and its role in potential adhesion formation after operative laparoscopy.
Design:
Randomized, controlled study (Canadian Task Force classification I).
Setting:
University-affiliated hospital.
Patients:
Twenty-eight women undergoing operative laparoscopy for adnexal masses.
Intervention:
For each patient, a 1 x 1-cm sidewall peritoneal flap was excised at the end of laparoscopy and numbered randomly. Similar flaps obtained from 24 women immediately after entering the abdomen during laparotomy served as controls.
Measurements and main results:
Changes in glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels were studied in homogenized peritoneal tissues. The duration of CO2 exposure and amount of CO2 used were correlated with levels of free radical scavengers and compared with controls. Mean CO2 exposure, amount of CO2 used, and CO2 pressure (15 mm Hg) was similar between low irrigation and irrigated laparoscopy (118.3 +/- 25 and 39.2 +/- 8.81 min and 125 +/- 20 and 44.5 +/- 6.81 min, respectively). The change in FRS levels was significantly correlated with duration and amount of CO2 exposure (r = -0.92). Levels of GSH-Px, SOD, CAT, and GSH were significantly lower in the CO2 exposure group than in controls (0.57 micro mol, 1.8 ng, 48.5 micro mol, 1.5 nmol vs 0.8 micro mol, 2.6 +/- 0.4 ng, 79 micro mol, 3.6 nmol, respectively).
Conclusion:
Exposure to CO2 has adverse effects on peritoneal microcirculation and cell-protective systems, which are proposed mechanisms in adhesion formation. Avoiding long CO2 exposure and copiously irrigating the abdominal cavity throughout surgery may lessen these effects. The potential role of the peritoneal FRS system on postoperative adhesion formation and its relation to estrogen status mandates further studies.
Acute increases in intraabdominal pressure (IAP) induce systemic and regional circulatory changes. Besides, mechanical compression on the capillary beds may decrease oxygen availability to the tissues. The purpose of this clinical study was to analyze the effects of increased IAP on acid-base disturbances and plasma lactate levels during prolonged carbon dioxide pneumoperitoneum.
Twenty-eight patients undergoing laparoscopic sigmoidectomy were included in this study. Fourteen of them (group A) had IAP of 15 +/- 1 mmHg while the remaining 14 (group B) had IAP of 10 +/- 1 mmHg. The control group included six patients undergoing conventional sigmoidectomy.
A progressive significant increase in PaCO2 was observed in the laparoscopic groups (p < 0.01). Plasma lactate levels in group A significantly increased 90 min after insufflation (p < 0.05) and reached the highest value 1 h after deflation (9.9 +/- 1 vs 31.9 +/- 2.5 mg/dl, p < 0.005). Simultaneously, arterial pH decreased in all groups; however, at 1 h after surgery, it was significantly lower (p = 0.02) in group A. There was a significant correlation between acid concentration due to lactate and lactate concentration (GA: R2 = 0.717, p = 0.03; GB: R2 = 0.879, p = 0.006 and GC: R2 = 0.853, p = 0.008).
High IAP causes lactic acidic accumulation in patients undergoing prolonged laparoscopic procedures.
Twelve ASA physical status I-II patients undergoing pelvic laparoscopy for infertility were enrolled in a study to quantify the effects of CO2 insufflation and the Trendelenburg position on CO2 elimination and pulmonary gas exchange, and to determine the minute ventilation required to maintain normocapnia during CO2 insufflation. Measurements of O2 uptake (VO2), CO2 elimination (VCO2), minute ventilation (VE), FIO2, and respiratory exchange ratio (RQ) were made during three steady states: control (C) taken after 15 min of normoventilation but before CO2 insufflation, after 15 min (L1) and 30 min (L2) of hyperventilation during CO2 insufflation. The FIO2 was controlled at 0.5 and arterial blood gases were used to calculate the oxygen tension-based indices of pulmonary gas exchange. After 15 min and 30 min of CO2 insufflation, the volume of CO2 absorbed from the peritoneal cavity was estimated at 42.1 +/- 5.1 and 38.6 +/- 6.6 (SEM) ml.min-1 respectively, increasing CO2 elimination through the lungs by about 30%. Hyperventilation of the lungs by a 20-30% increase in minute ventilation maintained normocapnia. Despite the CO2 pneumoperitoneum and Trendelenburg position, there was no impairment of pulmonary oxygen exchange as estimated by (A-alpha)DO2. This study demonstrated that a 30% increase in minute ventilation, achieved by increasing tidal volume to more than 10 ml.kg-1, is sufficient to eliminate the increased CO2 load and maintain normal pulmonary O2 exchange during pelvic laparoscopy.
Elevated intraabdominal pressure (IAP) occurs with intraabdominal bleeding, with tense ascites, or after application of military anti-shock trousers to trauma patients. While changes in renal perfusion with elevated IAP have been documented, there are no data available on blood flow to other viscera. Under pentobarbital anesthesia an inflatable bag was placed intraabdominally to create graded increases in IAP in 9 adult mongrel dogs (20 kg). Hemodynamic parameters and organ blood flow (OBF) using radioactive microspheres were measured at baseline and after increasing the IAP to 20 and 40 mm Hg. The organ blood flow index (OBFI = OBF/cardiac output) was determined for each organ (stomach, duodenum, jejunum, ileum, colon, pancreas, liver, spleen, kidney, and adrenal gland). Elevated IAP caused a decrease in OBF for all organs measured except the adrenal glands where the OBF was increased. The OBFI was decreased significantly for all intraabdominal viscera except the renal cortex and the adrenal gland. These changes in OBF are more marked than can be accounted for by changes in cardiac output alone, suggesting that local control mechanisms may be responsible for changes in OBF. Our data raise the possibility that elevation in IAP may result in visceral ischemia and organ dysfunction.
Subcutaneous and peritoneal tissue conductances for inert gases were measured in anesthetized Yorkshire piglets. Conductance spanned at least a 50-fold range in both subcutaneous and peritoneal tissues and showed the order: sulfur hexafluoride less than helium, neon less than ethylene less than nitrous oxide. Determination of conductance by measurement of composition changes within the gas space rather than the rate of pocket disappearance was particularly advantageous for the study of rapidly absorbed gases. Also, the simultaneous breathing of several inert gases substantially reduced interindividual variation by use of a reference gas. This study contains the first description of peritoneal gas exchange, including an estimate of effective peritoneal blood flow under conditions similar to laparoscopy. The critical role of diffusivity for discrimination between film and penetration models is discussed. More definitive modeling requires in vitro determination of tissue gas solubility and diffusivity.
The purpose of this experimental study was to determine the hemodynamic conditions of intraperitoneal viscera during pneumoperitoneum by using either CO2 gas or helium (He) for insufflation.
In 16 mongrel dogs (divided into a CO2 group and an He group) subjected to 14 mmHg pneumoperitoneum for 60 min, the following parameters were assessed at times before and 1, 2, 5, 15, 30, 45, and 60 min thereafter: (1) intestinal mucosal blood flow, by means of a laser-Doppler probe inplanted into a jejunal loop; (2) portal pressure and portal blood pCO2, through a catheter inserted via a mesenteric jejunal vein; (3) intramural jejunal pH (pHi), by means of a Tonometer, which expresses the degree of tissue ischemia; (4) inferior vena cava pressure and blood pCO2, through a catheter inserted via a femoral vein; and (5) from the systemic circulation pulse rate, arterial blood pressure, CO, CVP, PVP, SaO2, pCO2, and paO2 were measured through a catheter placed into a femoral artery and a Swan-Ganz thermodilution catheter inserted via the external jugular vein: CI and SVR were then calculated.
Jejunal mucosal blood flow was found decreased (P<0.0001) and pHi revealed gut mucosal ischemia. Portal and inferior vena cava pressures were found to be elevated (P<0.0001), as was blood pCO2 of these vessels (P<0.001), in only the CO2 group. From the systemic circulation, arterial blood pressure, CO, CI, SaO2, and paO2 revealed a decrease (P<0.001) while arterial pCO2 (only CO2 group), CVP, SVR, and PVP revealed an increase (P<0.001).
We conclude that severe hemodynamic alterations, not only to the systemic circulation but mainly to the viscera of the peritoneal cavity, are prominent after pneumoperitoneum for laparoscopic surgery. Elevation of portal and inferior vena cava pressures leads to splanchnic blood flow congestion and ischemia, while the use of CO2 seems to directly influence the pCO2.
The recent surge in enthusiasm for laparoscopic surgery has created concern that abdominal insufflation with carbon dioxide produces a respiratory acidosis. This may be because of both transperitoneal gas absorption and impaired ventilation with increased dead space from elevated intraabdominal pressure. To examine the relative contributions of these factors, we developed an animal model of surgical pneumoperitoneum that evaluated the cardiorespiratory effects of abdominal insufflation. Helium was chosen as an alternative to CO2 because it is both chemically and biologically inert. Carbon dioxide absorption during CO2 pneumoperitoneum caused arterial PCO2 to increase from 41.3 +/- 3.0 to a maximum of 58.3 +/- 4.0 mm Hg, with pH descending from 7.46 +/- 0.02 to a nadir of 7.31 +/- 0.02 (p < 0.05). Pulmonary artery pressure increased to twice baseline levels during CO2 insufflation (p < 0.05). Helium did not cause hypercarbia, acidemia, or pulmonary hypertension despite insufflation under identical conditions. These results indicate that transperitoneal absorption of CO2, not increased dead space, is responsible for the respiratory acidosis observed. Helium merits further study as an agent to induce pneumoperitoneum, especially when concerns of underlying acidosis or impaired gas exchange are present.
The effects of pneumoperitoneum with carbon dioxide and helium on systemic hemodynamics and arterial blood gases were investigated in pigs in an attempt to clarify the mechanisms by which pneumoperitoneum may induce organ dysfunction. A total of 16 anesthetized female pigs underwent pneumoperitoneum with carbon dioxide or helium (n = 8 each) in a stepwise fashion to intraabdominal pressures of 8, 10, 12, 16, and 20 mmHg. Changes in cardiac output; renal and hepatic blood flow; mean arterial, mean pulmonary arterial, mean pulmonary arterial wedge, inferior vena caval, and portal venous pressures; and total peripheral resistance were measured. Arterial blood samples were obtained at the same time the above parameters were determined. Urine volume was measured as an indicator of renal function. Pneumoperitoneum with either carbon dioxide or helium significantly increased venous pressures and simultaneously decreased cardiac output. These changes were associated with decreases in organ blood flow due to increased peripheral resistance. Urinary output was reduced to a similar degree in the two groups. Blood gas analysis revealed pneumoperitoneum-induced metabolic acidosis in both groups, although hypercapnia was observed only in the carbon dioxide group. These findings suggest that pneumoperitoneum-related organ dysfunction may be due to increased intraperitoneal pressure rather than to hypercapnia.
Carbon dioxide pneumoperitoneum has been shown to produce respiratory and hemodynamic changes due to both CO2 absorption and the effects of increased intraperitoneal pressure. We have measured the blood gas, end-tidal CO2, and hemodynamic changes produced during extraperitoneal CO2 insufflation (n = 22). These have been compared with the changes occurring during CO2 pneumoperitoneum (n = 11) under standardized anesthetic conditions. The changes observed during pneumoperitoneum were consistent with previous descriptions. There was a median rise in arterial pCO2 of 1 kPa over the first 15-20 min, followed by a second phase of only gradual change. There was also an increase in mean arterial pressure of 18 mmHg during the insufflation period. We have found a similar magnitude of rise in arterial pCO2 during extraperitoneal insufflation (median 0.83 kPa), but the rate of rise was significantly slower (P < 0.05). In addition, there was no change in the mean arterial pressure during extraperitoneal insufflation. Our results suggest that extraperitoneal CO2 insufflation may be safer than CO2 pneumoperitoneum in patients with preexisting cardiorespiratory disease.
Abdominal CO2 insufflation has been shown to cause hypercarbia, acidemia, and decreased oxygenation in a pediatric animal model. Such metabolic derangements have prompted a search for alternative insufflation gases. This study compares the hemodynamic and ventilatory changes that occur during pneumoperitoneum with CO2 and helium. Four juvenile swine were intubated and given general anesthesia. Minute ventilation was adjusted to obtain a baseline Pco2 of between 32 and 36 mm Hg, and was kept constant for the duration of the experiment. The subjects initially were insufflated with CO2 or helium at a pressure of 10 mm Hg. Peak ventilatory pressure, end-tidal CO2 (ETCO2) arterial pH, Pco2, Po2, and right atrial and inferior vena caval pressures were measured before and during a 1-hour insufflation period. After desufflation, Pco2 and pH were restabilized. The same parameters were then measured during reinsufflation with the alternate gas. CO2 insufflation caused significant decreases in pH, from 7.51 +/- 0.03 to 7.32 +/- 0.06, and Po2 increased from 261 +/- 49 to 189 +/- 33 mm Hg. Pco2 increased from 35.0 +/- 1.4 to 57.9 +/- 6.3 mm Hg. ETCO2 also increased, from 29.0 +/- 2.2 to 47.2 +/- 5.0 mm Hg. Helium insufflation caused pH to decrease from 7.51 +/- 0.01 to 7.42 +/- 0.04. Pco2 increased from 32.8 +/- 0.8 to 43.5 +/- 3.9 mm Hg, and ETCO2 increased from 27.8 +/- 0.5 to 36.8 +/- 3.1 mm Hg. These alterations were significantly less than those with CO2 pneumoperitoneum. Po2 decreased as well-from 266 +/- 30 to 212 +/- 21 mm Hg. During insufflation with both gases, peak ventilatory pressure and right atrial pressure increased significantly. Abdominal insufflation with CO2 or helium causes hypercarbia, acidemia, and increased ETCO2 in this juvenile animal model. These derangements are significantly less with helium. This gas may prove to be the more suitable insufflation agent for pediatric patients.
Port-site recurrences have often been reported after laparoscopic surgery for malignant disease, and the pathogenesis is unknown. Whether different gases used to establish pneumoperitoneum have an influence on tumor cell growth has not been investigated.
Tumor growth of colon adenocarcinoma DHD/K12/TRb was measured in a rat model after insufflation with either carbon dioxide or helium and in a control group. Tumor growth was evaluated in three experiments: (1) in vitro (n = 60), (2) ex vivo (n = 60), and (3) in vivo (n = 60). After insufflation, cell kinetics were determined in the first two experiments. In the third experiment, tumor growth was measured subcutaneously and intraperitoneally 5 weeks after insufflation.
Tumor cell growth increased significantly after insufflation with carbon dioxide in vitro (p < 0.03) and ex vivo (p < 0.05) compared with the control group, whereas helium did not stimulate cell growth. In vivo, subcutaneous tumor growth was promoted by carbon dioxide (131 +/- 55 mg) (p < 0.01) compared with helium (35 +/- 34 mg) and the control group (36 +/- 33 mg). Total intraperitoneal tumor weight was 717 +/- 320 mg in carbon dioxide group compared with helium (549 +/- 231 mg) and control group (570 +/- 321 mg).
The insufflation of carbon dioxide promotes tumor growth compared with helium and control in a rat model. Further studies should confirm these results before alternative gases should be recommended in laparoscopic surgery for malignant diseases.
Splanchnic macrocirculatory changes during high-pressure CO2 pneumoperitoneum include a decrease in mesenteric arterial blood flow, and decreased gastric perfusion with a drop in gastric pH in experimental studies. Microcirculatory changes in abdominal organs under clinical conditions with a low pressure CO2 pneumoperitoneum are unknown.
In 18 patients undergoing routine laparoscopy with a CO2 pneumoperitoneum (7 symptomatic cholecystolithiasis, 3 acute cholecystitis, and 8 acute appendicitis) gastric, duodenal, jejunal, colonic, hepatic, and peritoneal blood flow was measured with a custom-made laser Doppler flow probe at an intra-abdominal pressure of 0, 10, and 15 mm Hg.
Intra-abdominal pressure elevation from 10 mm Hg to 15 mm Hg significantly decreased the blood flow in the stomach by 40 percent to 54 percent, the jejunum by 32 percent, the colon by 44 percent, the liver by 39 percent, the parietal peritoneum by 60 percent, and the duodenum by 11 percent. Splanchnic blood flow decreased with operative time at a constant intra-arterial pressure (r = 0.88, p < 0.0001).
From our study, we concluded that laparoscopic procedures with a CO2 pneumoperitoneum should be performed at a pressure of 10 mm Hg or lower to avoid splanchnic microcirculatory disturbances.
Experimental studies demonstrated a severe cardiac load of the CO2 pneumoperitoneum caused by an accelerated after- and a decreased preload. Patients displaying cardiovascular risks are therefore often rejected from laparoscopic surgery. Hence, the pathophysiological changes and the intraoperative risk of the CO2 pneumoperitoneum in high-risk cardiopulmonary patients (NYHA II-III, n = 15) undergoing laparoscopic cholecystectomy are described. The changes in cardiac after- and preload seem to be due to the elevated intraabdominal pressure rather than transperitoneally resorbed CO2 and are reversible by desufflation. In one patient conversion to open operation had to be performed because of a severe drop in cardiac output and right ventricle ejection fraction. Mixed oxygen saturation was predicting intraoperative worsening in this case. The described pathophysiological changes may seem to be well tolerated even in high-risk cardiac patients. Monitoring of hemodynamics should include an arterial catheter line and blood gas analyses. Pharmacologic interventions or pressureless laparoscopic procedures might not be necessary as long as laparoscopic cholecystectomy is performed.
The purpose of this study was to investigate the effects of increasing intraabdominal pressure (IP) on gastric blood flow, as measured by gastric tonometry and traditional hemodynamic measurements.
Nine swine were anesthetized, intubated, and ventilated. Arterial and pulmonary artery catheters were placed by cutdown, a trocar was placed in the abdomen, and a gastric tonometer was placed in the stomach. Serial measurements of arterial and mixed venous blood gases, cardiac output, wedge pressure, lactic acid, and gastric intramucosal pH (pHi) were collected at intraperitoneal pressures of 0, 8, 10, 12, 14, 16, and 18 mm Hg after 30 min equilibration. Statistical analysis included Pearson correlation and Student's t test.
Increasing levels of IP were correlated with decreased arterial pH (p < 0.00003), increased mixed venous CO2 (p < 0.003), decreased intramucosal pH (p < 0.014), and increased arterial CO2 (p < 0.015). Gastric pHi differed significantly from baseline at IP levels of 16 mm Hg (p < 0.004) and 18 mm Hg (p < 0.01). No significant effects were observed on cardiac output or arterial lactate. No significant effects were observed in a control group that had been insufflated to 8 mm Hg and held constant over 3 h.
In this model, gastric blood flow is adversely affected by increasing i.p. with pronounced effects in excess of 15 mm Hg. These results suggest that gastric tonometry may be used to monitor the adverse effects of pneumoperitoneum. Gastric pHi may be an earlier indicator of altered hemodynamic function during laparoscopy than traditional measures.
Diagnostic laparoscopy has been used in abdominal trauma patients, although its role is not well defined. The safety of laparoscopic evaluation in trauma patients with severe intraabdominal hemorrhage has not yet been analyzed. The purpose of this study is to evaluate the hemodynamic and metabolic effects of CO2 pneumoperitoneum (COI) in hemorrhaged animals through a retroperitoneal hematoma (RH).
Twenty-two 15-20-kg mongrel dogs were monitored for systemic and pulmonary hemodynamics, inferior vena cava pressure, and arterial blood gases. After 1 h of baseline, all animals were submitted to a RH. After 45 min the dogs were randomized into two groups. Control (CTR): dogs were submitted only to a RH; pneumoperitoneum (PN): dogs were submitted to a RH and 45 min later they were insufflated to an intraabdominal pressure of 10 mmHg with medical-grade CO2 gas for 30 min. Echocardiography was performed, only in PN animals, at baseline, 45 and 60 min after RH.
RH induced a shock condition with low, sustained levels of arterial pressure, cardiac index, left ventricular stroke index, base excess, and oxygen delivery which were further depressed following COI. Three deaths occurred in the PN group, all of them toward the end of COI. During COI, hypercapnia was observed in one animal. COI did not impair systolic function or ejection fraction.
COI with an IAP of 10 mmHg may be deleterious in animals with hemorrhagic shock due to an intraabdominal lesion. These findings could be clinically significant in abdominal trauma patients.
Any route of entry into the abdomen contributes to alterations of the intraperitoneal organs with different clinical consequences. Characteristic alterations of the peritoneum after CO2 pneumoperitoneum used in laparoscopic surgery is examined.
A CO2 pneumoperitoneum with an intraperitoneal pressure of 6 mmHg was applied for 30 min in 32 nude mice. In the course of 4 days, the animals were killed and the peritoneal surface of the abdominal wall was studied by means of scanning electron microscopy.
Already 2 h after release of the pneumoperitoneum, mesothelial cells were bulging up. The intercellular clefts thereby increased in size, and the underlying basal lamina became visible. This reaction peaked after 12 h. Subsequently, peritoneal macrophages and lymphocytes filled all gaps, thereby recovering the basal lamina.
The morphologic integrity of the peritoneum is temporarily disturbed by a CO2 pneumoperitoneum.
The application of a CO2-pneumoperitoneum in operative laparoscopy presumably leads to basic alterations of the intraperitoneal homeostasis. In order to better understand the pathophysiology of this phenomenon, the morphologic alterations of the mesothelium after CO2-application will be examined.
In 36 mice (C 57, black mice) a CO2-pneumoperitoneum with an intraperitoneal pressure of 6 mm Hg was applied for 30 minutes. After 1, 2, 6, 12, 24, 48, 72 and 96 hours each of 4 animals were killed and the entire peritoneum was examined by scanning electron microscopy.
Already after 1 hour mesothelial cells became cuboidal, were detached and showed condensation. After 2 hours this initial reaction reached its peak; immature cells then attached to the free basal membrane. After 96 hours the entire mesothelium was regenerated.
The morphologic integrity of the mesothelium is temporarily disturbed by a CO2-pneumoperitoneum. Reasons for this phenomenon may be either the abdominal pressure or a CO2-induced surface acidosis. In further studies, the influence of the described phenomena on intraperitoneal formation of metastases will be examined.
30-67% of patients undergoing laparoscopic surgery reports shoulder pain. Besides, post-surgical course of patients undergoing converted laparoscopic procedures is similar to the course of patients who received a completely laparoscopic procedure. It is supposed that there is a temporary neurotoxic damage of the peritoneal sensitive nervous fibres defined by CO2.
A prospective review has been carried out by histologically analyzing 38 peritoneal biopsies from 10 selected patients, during different laparoscopic surgical procedures (6 cholecystectomies, 2 appendectomies, 1 selective bilateral ligature of the spermatic vessles) and at different times during each operation. Patients whom anamnesis, clinical or local conditions were suggestive for peritoneal flogosis were excluded from the study: therefore only 29 biopsies from 8 patients have been considered useful to the study.
Histological analysis has been carried out with different methods of coloration (hematoxylin eosin, argentic staining) and at different magnifications (30x, 60x, 100x), without electronical microscopy or immunohistochemical studies. No biopsy showed signs of damage of the nervous structures.
Certainly, the realization of a pneumoperitoneum at CO2 doesn't cause damages of the peritoneal sensitive fibres. It has been demonstrated that the abdominal introduction of CO2 causes a "relative peritoneal acidosis", directly depending from the percentage of CO2 employed: the peritoneal pH decreases to 6.9 after 15 min of pneumoperitoneum with CO2 at 100% and to 7.35% with CO2 at 5% of air. Probably this condition causes a temporary biochemical change that defines reduction of the nervous impulses and, therefore, the "peritoneization" of the patient subjected to laparoscopic procedure. The "biochemical hypoesthesia", based on a change of the peritoneal homeostasis, would translate itself in a beneficial effect for the patient, persisting also when converted to laparotomic operation due the impossibility to proceed under laparoscopy, held up by the residual pneumoperitoneum.
Although there have been studies of the effects of pneumoperitoneum on the peritoneal cavity, we still do not know whether the morphologic changes to the peritoneum are different for pneumoperitoneum vs laparotomy. Using scanning electron microscopy, we examined the murine peritoneum after pneumoperitoneum vs laparotomy and compared the changes.
Forty-five mice were anesthetized with diethyl ether and divided into seven groups. Pneumoperitoneum was established at 5 mmHg for 30 min with carbon dioxide (CO(2)) (n = 9), helium (n = 9), and air (n = 9). One group underwent laparotomy for 30 min (n = 9), and a control group underwent anesthesia only (n = 3). CO(2) pneumoperitoneum was further established at 10 mmHg for 30 min (n = 3) and at 5 mmHg for 60 min (n = 3). After the procedures, the peritoneum was resected from the mesenterium of the small intestine in each animal and examined by scanning electron microscope for morphologic changes of the mesothelial cells.
Bulging up of the mesothelial cells was evident immediately after pneumoperitoneum, whereas detachment of the mesothelial cells was present immediately after laparotomy. Bulging up of the mesothelial cells was reduced at 24 h after CO(2) pneumoperitoneum and fully resolved at 72 h in all pneumoperitoneum groups, whereas the mesothelial cells remained detached at 72 h in the laparotomy group. Intercellular clefts were found immediately after helium pneumoperitoneum and were present at 24 h and 72 h after helium pneumoperitoneum, but they were not seen after air pneumoperitoneum and were only evident after CO(2) pneumoperitoneum at 10 mmHg. Depression of the mesothelial cell surface was observed when pneumoperitoneum lasted 60 min.
Morphologic peritoneal alterations after pneumoperitoneum differed from those after laparotomy and were influenced by the type of gas, amount of pressure, and duration of insufflation. These peritoneal changes after pneumoperitoneum may be associated with a specific intraperitoneal tumor spread after laparoscopic cancer surgery.
To develop a laparoscopic mouse model to evaluate the hypothesis that mesothelial hypoxia during pneumoperitoneum is a cofactor in adhesion formation.
Prospective randomized trials.
Academic research center.
One hundred thirty female Naval Medical Research Institute (NMRI) mice.
Adhesions were induced by opposing monopolar lesions in uterine horns and pelvic side walls during laparoscopy and evaluated after 7 or 28 days under microscopic vision during laparotomy. The following pneumoperitoneum variables were assessed: duration (10 or 60 minutes), insufflation pressure (5 or 15 cm of water), insufflation gas (CO(2) or helium), and addition of oxygen (0-12%).
Adhesions were scored quantitatively and qualitatively for extent, type, and tenacity.
Scoring of adhesions 7 or 28 days after laparoscopic surgery was comparable. Adhesions increased with duration of pneumoperitoneum and with insufflation pressure and decreased with the addition of oxygen. Half-maximal reduction of adhesions was obtained at 1.5% oxygen, whereas a maximal reduction required only 2%-3%. The effect of CO(2) and helium was similar.
These data demonstrate the feasibility of the intubated laparoscopic mouse model and confirm previous observations in rabbits, indicating that mesothelial hypoxia plays a key role in adhesion formation.
Port site metastasis is a well-documented event after laparoscopic procedures in cancer patients. We summarize current epidemiological knowledge about the risk of this complication after laparoscopic/conventional cholecystectomy in patients with unexpected gallbladder cancer as well as other intraabdominal malignancies. We found 174 cases of port site metastasis after laparoscopic cholecystectomy and 12 recurrences in the surgical scar after converted or open cholecystectomy. A review of all case reports and its comparison with four international surveys show a 14% incidence of port site metastases 7 months after laparoscopic cholecystectomy for cancer. Similar numbers are available for open cholecystectomy. Our data suggest that abdominal wall metastases of gallbladder cancer are not a specific complication of laparoscopy. The long-term prognosis of patients with unknown gallbladder cancer however seems to be worsened by laparoscopy. The registry of the German Society of Surgery, which prospectively compares follow-up and prognosis of all cases of cholecystectomy, laparoscopic as well as open, in patients with incidental gallbladder cancer will definitively clarify whether laparoscopy affects the prognosis of patients with unsuspected gallbladder cancer.
To investigate the effects of carbon dioxide (CO(2)) pneumoperitoneum-induced changes in blood gases, acid-base balance, and oxygen homeostasis in rabbits.
Prospective, randomized, controlled study (Canadian Task Force classification I).
University training and teaching center.
Twenty-six adult female New Zealand white rabbits.
Anesthesia and pneumoperitoneum.
In anesthetized rabbits arterial blood gases, acid-base balance, oxygenation values, and lactate concentrations were assayed during 2 hours. Spontaneous breathing, superficial and optimal ventilation without pneumoperitoneum, and with pneumoperitoneum at low (6 mm Hg) and higher (10 mm Hg) insufflation pressures were compared. The CO(2) pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis. Carboxemia with increasing end-tidal CO(2) and partial pressure of CO(2) (p <0.001), acidosis with decreasing pH (p <0.001), and base deficiency with decreasing actual base excess (p <0.001), standard base excess and standard bicarbonate and acid excess with increasing hydrogen bicarbonate (p <0.05 and <0.01) were found. Desaturation (p <0.01) with decreasing oxyhemoglobin p <0.05) and hemoglobin oxygen affinity (p <0.01) were also found. Carboxemia with acidosis was more pronounced with higher (p <0.01) than with lower (p >0.05) intraperitoneal pressures, and also with spontaneous breathing (p <0.05) and superficial ventilation (p <0.001) than with optimal ventilation, resulting in metabolic hypoxemia.
In superficially ventilated and spontaneously breathing rabbits, CO(2) pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis, resulting in metabolic hypoxemia. With optimal ventilation and low intraperitoneal pressure carboxemia, respiratory acidosis, and changes in oxygen metabolism were minimal.
Several experimental studies confirm the hypotheses that laparoscopic gases influence the development of tumor metastases [12, 14, 23]. The mechanism for this alteration of malignant tumor growth is still unknown. One reason might be an influence of the in sufflation gas on essential cell function regulating parameters. To investigate the changes of the intra- and extracellular milieu, four parameters--extra- and intracellular pH, intracellular free calcium levels, and tissue oxygen partial pressure--were measured during insufflation with carbon dioxide (CO2), helium (He), or a nonhypoxic gas mixture consistent of 80% CO2 and 20% O2.
(In vitro experiments) Intracellular calcium and pH levels were measured in DHD/K12/TRb colon adenocarcinoma cells using fluorescence imaging microscopy. (In vivo experiments) Tissue oxygen partial pressure was measured using a flexible micro catheter (Licox CMP) implanted in the abdominal wall of rats. After establishing the pneumoperitoneum an optical system and an aspirator were inserted to control the position of the micro catheter and to aspirate wound exudates for pH measurements of the wound fluid.
Creating of pneumoperitoneum with both CO2 and helium caused a decrease in partial pressure of oxygen in the abdominal wall to about 5 mm Hg whereas insufflation with a nonhypoxic gas mixture (80% CO2 and 20% O2) induced no significant changes. The intra- and extra cellular pH values dramatically decreased during CO2 insufflation (7.4 to 6.2) in vitro. Helium caused a pH increase up to 7.6. Free intracellular calcium was enhanced during CO2 insufflation, whereas helium insufflation did not cause any changes in [Ca2+]i. Nevertheless, a significant decrease of [Ca2+]i was observed during reoxygenation following helium-induced hypoxia.
Our study demonstrates that insufflation with either CO2 or He causes significant changes of intra- and extracellular parameters regulating essential cell functions such as oxidative phosphorylation to produce ATP, cell proliferation, or onset of apoptosis.
To identify oxidative stress in peritoneum during laparoscopic and open surgery by measuring products of lipid peroxidation, and to determine whether surgical approach influences the type of oxidative metabolite synthesized.
Retrospective analysis (Canadian Task Force classification II-2).
University-affiliated hospital.
Twenty-eight consecutive women with uterine myomas or ovarian cysts.
Laparoscopic or open surgery (14 patients each).
We obtained 1 x 1-cm squares of peritoneum at the beginning and end of surgical procedures away from sites of surgery. 8-Isoprostaglandin F(2alpha), hydroxyeicosatetranoic acids (HETEs), and malondyaldehyde (MDA) were measured by enzyme-immunoassay, high-performance liquid chromatography, and thiobarbituric acid adduction method, respectively. Comparisons showed significant increases in 5-HETE and 8-prostane in the laparoscopy group, which were correlated with duration of pneumoperitoneum and volume of carbon dioxide (CO(2)) insufflated, respectively. In the laparotomy group only MDA rose significantly related to duration of surgery.
Lipid peroxidation was observed in peripheral peritoneum during laparoscopic surgery, mediated through noncyclooxygenase and lipoxygenase pathways, and appears to be due to effects of CO(2) pneumoperitoneum. Biochemical reactions were also observed in the laparotomy group, but are thought to be related to mechanisms other than lipid peroxidation.
To evaluate the role of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in adhesion formation after laparoscopic surgery.
Prospective, randomized study.
Academic research center.
Female wild-type mice and transgenic mice (n = 110), expressing exclusively VEGF-A(164) (VEGF-A(164/164)) or deficient for VEGF-B (VEGF-B(-/-)) or for PlGF (PlGF(-/-)).
Adhesions were induced during laparoscopy. To evaluate "basal adhesions" and "CO(2) pneumoperitoneum-enhanced adhesions," the pneumoperitoneum was maintained for a minimum (10 minutes) or prolonged (60 minutes) period. The role of PlGF was also evaluated by administration of antibodies.
Adhesions were blindly scored after 7 days.
In all wild-type mice, CO(2) pneumoperitoneum enhanced adhesion formation. In comparison with wild-type mice, basal adhesions were higher in VEGF-A(164/164) mice and similar in VEGF-B(-/-) and PlGF(-/-) mice. Pneumoperitoneum did not enhance adhesions in any of these transgenic mice. The effects observed in PlGF(-/-) mice were confirmed in PlGF antibody-treated mice.
The data demonstrate that the VEGF family plays a role in adhesion formation and confirm that CO(2) pneumoperitoneum enhances adhesions. VEGF-A(164) has a direct role in basal adhesions. Absence of pneumoperitoneum-enhanced adhesions in VEGF-A(164/164), VEGF-B(-/-), and PlGF(-/-) mice indicates up-regulation of VEGF-A(164), VEGF-B, and PlGF by CO(2) pneumoperitoneum as a mechanism for pneumoperitoneum-enhanced adhesion formation.
Little is know about the effects of different insufflation gases on peritoneal pH during laparoscopy. However, these changes may influence the intracellular signalling system, resulting in altered cell growth or adhesiveness. The aim of this study was to determine the effects of carbon dioxide (CO(2)), nitrous oxide (N(2)O), and helium (He) on parietal and visceral peritoneal pH. The effect of different intraabdominal pressures on parietal and visceral peritoneal pH was also examined.
We conducted both an ambient gas study and a pressure study. For the ambient gas study, 20 pigs were divided into the following four groups: (a) CO(2), (b) He, (c) N(2)O, and (d) abdominal wall lift (Lift) laparoscopy. Parietal and visceral peritoneal pH were measured at 15 min intervals for 180 min. For the pressure study, 15 pigs were divided into the following three groups: (a) CO(2), (b) He, (c) N(2)O laparoscopy. Baseline values were established for parietal and visceral peritoneal pH. Intraabdominal pressure was then increased stepwise at 1-mmHg intervals to 15 mmHg. After pressure was maintained for 15 min at each setting, parietal and visceral peritoneal pH were measured.
Ambient gas environment was the major determinant of parietal peritoneal pH. Carbon dioxide caused parietal peritoneal acidosis. Helium, N(2)O, and Lift caused alkalotic parietal peritoneal pH. Intraabdominal pressure had a minor effect on parietal peritoneal pH. At higher intraabdominal pressure (12-15 vs 5-8 mmHg), CO(2) caused a slight decrease in parietal peritoneal pH, whereas N(2)O and He caused a slight increase in parietal peritoneal pH. Visceral peritoneal pH remained relatively unaffected during all studies.
Parietal peritoneal pH during laparoscopy was highly dependent on the ambient gas environment. The effect of intraabdominal pressure on parietal peritoneal pH was of minor significance. Carbon dioxide caused a slight worsening of parietal peritoneal acidosis at higher intraabdominal pressure, whereas, N(2)O, He, and Lift did not cause parietal peritoneal acidosis.
Carbon dioxide (CO(2)) is the most common gas used for insufflation in laparoscopy, but its effects on peritoneal physiology are poorly understood. This study looks at the changes in peritoneal and bowel serosal pH during CO(2) pneumoperitoneum, and whether heating and humidification with or without bicarbonate alters the outcomes.
Twenty-one pigs divided into four groups as follows: (1) standard (STD) laparoscopy (n = 5); (2) heated and humidified (HH) laparoscopy (n = 6); (3) heated and humidified with bicarbonate (HHBI) laparoscopy (n = 5); and (4) laparotomy (n = 5). Peritoneal pH, bowel serosal pH, and arterial blood gas (ABG) were obtained at 15-min intervals for 3 h.
Severe peritoneal acidosis (pH range 6.59-6.74) was observed in all laparoscopy groups, and this was unaltered by heating and humidification or the addition of bicarbonate. Bowel serosal acidosis was observed in all laparoscopy groups with onset of pneumoperitoneum, but it recovered after 45 minutes. No significant changes in peritoneal or bowel serosal pH were observed in the laparotomy group.
CO(2) pneumoperitoneum resulted in severe peritoneal acidosis that was unaltered by heating and humidification with or without bicarbonate. Alteration in peritoneal pH may conceivably be responsible for providing an environment favorable for tumor-cell implantation during laparoscopy.
Open laparoscopy was used to diagnose advanced ovarian cancer. Patients with a pelvic mass and an omental cake and/or large-volume ascites were selected for open laparoscopy. One hundred and seventy-three patients with stage III or IV ovarian carcinoma underwent diagnostic open laparoscopy. Seventy-one patients underwent complete excision of port sites at the time of debulking surgery. Thirty (17%) patients developed port-site metastases. However, only 8 (5%) of these port-site metastases were clinically diagnosed, while 22 out of 71 (31%) with complete port-site excision were diagnosed on pathologic examination. There was no significant relationship between the development of port-site metastases and median time to primary chemotherapy or surgery, the presence of ascites, or stage IV disease. All port-site metastases disappeared during primary therapy, and none of the patients developed a second relapse in one of their port sites. We observed a high rate of port-site metastases after laparoscopy in patients with advanced ovarian carcinoma. However, prognosis was not worse in this group of patients. Laparoscopy is a convenient technique to diagnose advanced ovarian carcinoma, to exclude other primary tumors, and to refer patients to a tertiary center.
Previous animal studies suggested that the peritoneal environment during a carbon dioxide (CO(2)) pneumoperitoneum is hypoxic and that this may contribute to the formation of intra-abdominal adhesions or the growth of malignant cells. There is no study, however, that investigates the relationship between anaesthesia, ventilation and the laparoscopic peritoneal environment to the development of hypoxia. The objective of this study is to monitor the peritoneal tissue-oxygen tension (PitO(2)) under various conditions including anaesthesia alone, during a CO(2) pneumoperitoneum at both low and high intraperitoneal pressure (IPP), and laparotomy, in animal models with controlled respiratory support (CRS).
C57BL6 mice were divided into eight groups (n = 5) consisting of anaesthesia alone or with CO(2) pneumoperitoneum at low (2 mmHg) or high (8 mmHg) IPP or undergoing laparotomy. Groups were further subdivided into those with or without CRS with endotracheal intubation and mechanical ventilation. Over the course of the 1 h procedure, PitO(2) was continuously monitored.
Protocol 1. The PitO(2) levels (104.2 +/- 7.8 mmHg, mean +/- SEM) in non-injured peritoneum during a CO(2) pneumoperitoneum at a low IPP were elevated approximately 2-fold over the levels during laparotomy (49.8 +/- 15.0 mmHg) in ventilated mice. Protocol 2. After insufflation with CO(2), the PitO(2) was immediately elevated and maintained at a higher level. Following laparotomy, it decreased immediately. This elevation was not seen with air insufflation.
In mice, a significant elevation in PitO(2) occurs during a CO(2) pneumoperitoneum at low IPP with CRS.
Carbon dioxide pneumoperitoneum induces peritoneal oxidative stress. The aim of this study was to verify the effect of intra-abdominal pressure on oxidative stress in the peritoneum and on post-operative adhesion formation.
Forty-one rabbits underwent laparoscopic surgery: either gasless, or with CO(2)-pneumoperitoneum at pressures of 5, 10 or 15 mmHg. Serial parietal peritoneal biopsies were taken at various time-points: immediately after reaching the abdominal cavity, 30, 60, 90 and 120 min afterwards, and 15 min after abdominal desufflation. 8-iso prostaglandin F(2alpha) (8-iso PGF(2alpha)), a marker of oxidative stresss, was assayed by enzyme immunoassay and adhesion formation was scored by second-look laparoscopy on day 14.
The gasless group showed no significant changes in 8-iso PGF(2alpha). Conversely, significant changes occurred in CO(2)-pneumoperitoneum in a time- and pressure-dependent manner. Adhesions developed only in the CO(2)-pneumoperitoneum groups, and total adhesion score was correlated with the amount of CO(2) insufflated and intra-abdominal pressure, but not with 8-iso PGF(2alpha), which was correlated with intra-abdominal pressure.
Intra-abdominal pressure increased 8-iso PGF(2alpha) in the parietal peritoneum in a graded fashion, whilst gasless laparoscopy had no impact. It also influenced the frequency and severity of adhesion formation, but no causal link was found between 8-iso PGF(2alpha) and post-operative adhesion formation.
Theeffectsofpneumo-peritoneum ongastric bloodflow andtraditionalhemodynamic measure-ments
- Knolmayertj
- Bowyermw
- Eganjc
KnolmayerTJ,BowyerMW,EganJC,AsbunHJ.Theeffectsofpneumo-peritoneum ongastric bloodflow andtraditionalhemodynamic measure-ments. Surg Endosc 1998;12:115–8
Effect of extraperito-nealcarbondioxideinsufflationonintraoperativebloodgasandhemody-namic changes
- Dm Wright
- Mg Serpell
- O Jn Baxter
- Dwyer
Wright DM, Serpell MG, Baxter JN, O’Dwyer PJ. Effect of extraperito-nealcarbondioxideinsufflationonintraoperativebloodgasandhemody-namic changes. Surg Endosc 1995;9:1169–72.
Effectsof supplemental perioperative oxygen on post-operative abdominal wound adhesions in a mouse laparotomy model with controlled respiratory sup-port 784 Mynbaev et al. Ventilation-related metabolic changes
- Matsuzakis
- Canism
- Bazinje
- Darchac
- Poulyjl
- Mageg
MatsuzakiS,CanisM,BazinJE,DarchaC,PoulyJL,MageG.Effectsof supplemental perioperative oxygen on post-operative abdominal wound adhesions in a mouse laparotomy model with controlled respiratory sup-port. Hum Reprod 2007;22:2702–6. 784 Mynbaev et al. Ventilation-related metabolic changes Vol. 92, No. 2, August 2009
Ventilation-related metabolic changes
- Mynbaev
Mynbaev et al. Ventilation-related metabolic changes Vol. 92, No. 2, August 2009
Transplanted cancer cell metastatic syndrome in the peri-toneum wounds or/and port-sites: Russian roulette in surgical oncology [thesis]
- Mynbaev
- Oa
Mynbaev OA. Transplanted cancer cell metastatic syndrome in the peri-toneum wounds or/and port-sites: Russian roulette in surgical oncology [thesis]. Vrij Universiteit Brussel (VUB) and Ghent University. Brussels-Ghent, Belgium 2006;1–87.
Carbon dioxide pneumo-peritoneum causes severe peritoneal acidosis, unaltered by heating, Fertility and Sterility â humidification, or bicarbonate in a porcine model
- Wong Yt
- Pc Shah
- Birkett Dh
- Dm
Wong YT, Shah PC, Birkett DH, Brams DM. Carbon dioxide pneumo-peritoneum causes severe peritoneal acidosis, unaltered by heating, Fertility and Sterility â humidification, or bicarbonate in a porcine model. Surg Endosc 2004;18: 1498–503.
The oxygen cascade. Nunn's applied respiratory physiology
- Jf Nunn
Nunn JF. The oxygen cascade. Nunn's applied respiratory physiology. 4th ed. Oxford: Butterworth-Heinemann, 1993;260–7.