The advantages of diagnostic laparoscopy in portal hypertensive (PHT) patients include visual examination of the liver, regional collateralization, and obtaining liver biopsy specimens directly from the nodular structures. However, laparoscopic investigation, which is performed with the use of CO2 insufflation into the peritoneal cavity, is not without potential complications. In 1993, we recognized that the Paco2 levels of PHT patients were remarkably higher than those of systemically healthy children, for instance, patients with undescended testis. Changes in arterial CO2 (Paco2) and the hemodynamic state that occurs during laparoscopic procedures have been extensively studied in adult patients (1,2). Several factors have been considered as responsible for the hypercarbia encountered during diagnostic or interventional laparoscopic procedures. These factors include absorption of CO2 by the peritoneum, alterations in cardiac output and respiratory mechanics and function caused by increased intraabdominal pressure, and cephalad displacement of the diaphragm, resulting in decreases in lung volume and functional residual capacity (1–7). The aim of this study was to verify the differences arising from changes in blood gases in two groups of children undergoing laparoscopic procedures: 1) PHT patients and 2) children who were otherwise in reasonably good health (the control group).
Fifty-seven children, ranging in age from 2 to 14 yr, who were scheduled for laparoscopic procedures were enrolled in this prospective, observational study after institutional ethics committee approval and informed parental consent were obtained. The patients were divided into two groups (the PHT group and the control group) according to the following criteria: patients with a negative history for systemic pathologic events and who were otherwise healthy during physical examination were considered normal, healthy children (the control group), with an ASA physical status of I or IE. The patients with PHT (the PHT group) were diagnosed with impaired liver function, esophageal variceal bleeding, and hepato- and/or splenomegaly, as evidenced by liver ultrasound, portal scintigraphy, and computed tomography (8,9). The PHT patients had ASA scores of II and III. Preoperative diagnoses of these patients were verified by the laparoscopic views and biopsies reported during the study.
After 6 h of fasting, the children from both groups, all unpremedicated, were taken to the operating room. Electrocardiogram, noninvasive blood pressure, and Spo2 (Datex Capnomac; Datex-Ohmeda, Helsinki, Finland) were monitored. For both groups, anesthesia was induced with thiopental 5 mg/kg and atracurium 0.5 mg/kg. After tracheal intubation with an appropriately sized endotracheal tube, general anesthesia was maintained with isoflurane (expiratory concentration 1.5%) in 50% oxygen in air. The control group received morphine 0.1 mg/kg; the PHT group received 2 μg/kg of fentanyl during the induction of anesthesia, and this was repeated as required. The infusion regimen was composed of lactated Ringer’s solution for the control group and physiologic saline for the PHT group, calculated ac-cording to a 4-2-1 formula (4 mL · kg−1 · h−1 for the first 10 kg plus 2 mL · kg−1 · h−1 for the next 10 kg plus 1 mL · kg−1 · h−1 thereafter) during laparoscopy. Neo-stigmine 40 μg/kg and atropine 20 μg/kg were administered for the reversal of neuromuscular blockade at the end of the procedure.
End-tidal CO2 (ETco2) monitoring was initiated. The Sulla 808 V (Draeger, Lubeck, Germany) volume-controlled (constant flow) ventilator with pediatric hoses was used for all patients. Ventilatory management included an exhaled tidal volume of 10 mL/kg, and the initial rate was adjusted to achieve an ETco2 concentration of 30–38 mm Hg. The inspiratory/expiratory time ratio was 1:2 without positive end-expiratory pressure. Minute ventilation and tidal volume was monitored by a spirometer placed in the expiratory limb of the breathing system. The initial ventilatory settings were not altered unless ETco2 and Paco2 reached 55 and 60 mm Hg, respectively, during pneumoperitoneum.
During laparoscopy procedures, the abdominal pressure was displayed and automatically maintained at 8–12 mm Hg by using a Storz (Tutlingen, Germany) electronic laparoflator. A nasogastric tube and urinary catheter were placed in all patients. All patients lay supine, with no tilt of the table.
An intraarterial cannula was inserted into the radial artery for blood sampling. If the first attempt for putting in an arterial line was not successful, further attempts were not attempted, and the patient was excluded from the study. Heparinized blood samples were collected before pneumoperitoneum (T0), at 15 and 30 min during pneumoperitoneum (T15 and T30), after desufflation (Tend), and 10 min after extubation (Text). Blood gases were immediately measured with the Ciba Corning 860 blood gas analyzer. The heart rate (HR), mean arterial blood pressures (MAP), ETco2, and Spo2 were recorded at T0, 1 min after pneumoperitoneum (T1), T15, T30, Tend, and Text.
Statistical power analysis with an α error of 0.05 and a β of 95% indicated that 22 patients for each group would be necessary to detect a difference of 5 mm Hg in Paco2 between groups, with an sd of 4.5, according to previous studies performed by the same department (10). Analysis of variance (ANOVA) for repeated measurements was used for evaluating changes within the groups, and χ2 and Student’s t-tests were performed comparing differences between the control and PHT groups. Correlation analysis was performed for evaluating the relationship between Paco2 and ETco2. Student’s t-test was applied for comparing the Paco2 and pH changes of extrahepatic and intrahepatic PHT patients. P < 0.05 was considered statistically significant. A correlation ratio of 0.80–1.00 was considered a good correlation.
Demographic data of the patients are presented in Table 1. The groups were different in respect to the duration of anesthesia and pneumoperitoneum. The duration of anesthesia was almost triple the pneumoperitoneum duration in both groups. In the control group, some patients had circumcision; other control group patients with testis in the inguinal canal or vanishing testis underwent inguinal-scrotal exploration. Patients with PHT had sclerotherapy after laparoscopy.
Throughout the study, the HR and MAP did not show great variability in either group (ANOVA for repeated measurements;P > 0.05) (Table 2). In the control group, four patients had increased HR to >20% at the first minute of pneumoperitoneum. Two patients in the control group developed ventricular ectopic beats at 12 mm Hg intraabdominal pressure; one patient developed bradycardia; and another had Wenckebach rhythm before surgery, recovered after the induction of anesthesia, and had no problems during anesthesia. In the PHT group, one patient had a history of an atrial septal defect correction; this patient’s ductus arteriosus was patent at the time of laparoscopy. Another patient developed transient tachycardia at T1. At the first minute of pneumoperitoneum, two patients had an increase and two had a decrease in MAP in the control group, whereas in the PHT group, two patients had an increase and three patients had a decrease in MAP. There was no statistical significance between groups regarding changes in HR and MAP.
The changes of Paco2, pH, and ETco2 were statistically significant during the study periods in both groups (ANOVA for repeated measurements;P < 0.05) (Fig. 1). The percentage of Paco2 increase between T0 and T15 was 11.5% (sd, 17.3%) and 20.1% (sd, 13%), respectively, in the control and PHT groups (P < 0.05). This increase reached 36.8% at T30 in the PHT group (n = 13), whereas the control group had a 17.2% increase at T30 (n = 23) compared with T0 (P < 0.05). The Paco2 increased to >60 mm Hg in three patients at T30 (n = 13) in the PHT group (χ2;P < 0.05). These patients were ventilated manually to quickly remove CO2. The hemodynamics were not affected in these three patients, and only one of them had profound sweating. The changes in ETco2 were in good correlation with the changes in Paco2 (r = 0.8133). The variability in base excess, bicarbonate, Pao2, arterial oxygen saturation, and Spo2 during the study periods was not statistically significant in either group (ANOVA for repeated measurements;P > 0.05) (Table 3). There was no evidence of hypoxemia in any patient: arterial oxygen saturation and Spo2 were never less than 94%. The initial (T0) Pao2 was 281.9 ± 64.1 mm Hg and 229.7 ± 61.4 mm Hg in the control and PHT groups, respectively. The initial pH and base excess were also significantly lower in the PHT group than the control group (Fig. 1). The comparisons between extrahepatic and intrahepatic PHT children in respect to Paco2 and pH did not reveal a significant difference (P > 0.05).
The minimal alterations in the HR and MAP during laparoscopic procedures in this study could be attributed to limiting intraabdominal pressure to 12 mm Hg and avoiding position changes (4,5,11). Although the Paco2 increase was remarkable during pneumoperitoneum in the PHT group, the hemodynamic alterations caused by hypercarbia were not prominent. Underlying liver disease, which enables a reduced responsiveness of the cardiovascular system to sympathetic discharge or catecholamines, might have had some consequences on this outcome in the PHT group (12). The changes in rhythm at the beginning of pneumoperitoneum could be attributed to sudden abdominal distention, vagal stimulation, or inadequacy of analgesia at that moment in both groups.
The diffusion of CO2 into the vascular system through the peritoneum with the use of CO2 for pneumoperitoneum is inevitable. The CO2 diffuses rapidly into the tissues when a very small pressure difference occurs. During a laparoscopic procedure, CO2 diffuses into the abdominal organs and then passes into the bloodstream, in addition to the direct diffusion into the blood through the peritoneal surface (13). Several authors have reported an increase in CO2 load of 30%–40% during pneumoperitoneum, which was thought to be caused by absorption of CO2 from the abdominal cavity (14,15). Pennant (11) stated that in children, CO2 uptake is more efficient because of the smaller distance between capillaries and peritoneum and the larger absorptive area of the peritoneum in relation to body weight. The CO2 increase in children is usually within clinically tolerable limits (3,10,16–18). According to Fick’s law of diffusion for CO2:MATH where ΦCO2 is CO2 flux, D is the diffusivity of CO2 between the peritoneal cavity and the blood, A is the area of peritoneum exposed to CO2, d is the distance between the peritoneal surface and blood, Ppco2 is the partial pressure of CO2 in the peritoneum, and Pbco2 is the partial pressure of CO2 in the blood (19).
The major difference between the healthy individuals and those with PHT is the difference in the surface area of peritoneum exposed to insufflated CO2 content (A). In the children with PHT, unlike the healthy children, the visceral and parietal peritoneum surfaces are increased by engorgement of the portal vein and a number of enlarged and tortuous collateral venous developments in the parietal and visceral peritoneal surfaces and arteriovenous vascular structures, angiomatous development on the liver surface, and enlargement of liver and spleen (8,9). Additional pathophysiologic processes in PHT that greatly contribute to CO2 absorption are the dilated, tortuous, and thin-walled collateral vessels, a decrease in peripheral vascular resistance, increased plasma volume, increased flow in the splanchnic arterial system, hyperdynamic circulation, and increased cardiac output (12,20). The increase of collateral vessels, which have thinner walls, decreases the distance between the peritoneal surface and blood (d).
Interestingly, despite the locations of collaterals and the differences in portal blood volume in extrahepatic and intrahepatic PHT patients, we were unable to find any differences in Paco2 values between these two groups of PHT patients undergoing diagnostic laparoscopic procedures (9). This outcome might also be attributed to Type II statistical error, with the number of patients with the diagnosis of extrahepatic and intrahepatic PHT being 12 and 16, respectively.
Findings of high Paco2 and low pH in this study were well correlated because of the unchanged bicarbonate level throughout the procedure. Both Paco2 and pH immediately recovered and turned back to the preinsufflation values with the release of the pneumoperitoneum. One of the consequences of liver disease and PHT is pulmonary dysfunction, which presented as an initially low Pao2 in the PHT group, despite the fixed fraction of inspired oxygen in all patients (21–23). Another explanation for a small high Paco2 and significantly low Pao2 in the PHT group could be the difficulty of ventilation because of enlarged spleen, liver, or both. Although it had been reported that Pao2 was reduced throughout pneumoperitoneum because of a reduction in compliance, leading to a diminished functional residual capacity relative to closing volume, this finding was not clinically relevant in our study (24,25). A high fraction of inspired oxygen (50%) applied during laparoscopy prevented clinical hypoxia from developing, even in pulmonary dysfunction.
In conclusion, the rate of increase of Paco2 was greater in children with PHT compared with normal children. ETco2 monitoring reflected these increases. Anesthesiologists need to be more vigilant in PHT patients in terms of continuously reassessing the adequacy of ventilation and the resultant effects and the ETco2.
The authors thank David Chasey, editorial assistant, Department of Anesthesiology, Children’s Hospital of Pittsburgh, for his review of the manuscript. We also thank the following pediatric surgeons for their cooperation: Drs. N. Danismend, C. Buyukunal, Y. Soylet, and E. Erdogan.
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