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PEDIATRIC ANESTHESIA

The Effect of Insufflation Pressure on CO₂ Pneumoperitoneum and Embolism in Piglets

David S. Beebe, MD^*, Shoumin Zhu, MD PhD^*, M. V. Shailesh Kumar, PhD^*, Vijaya Komanduri, MS^*, John A. Reichert, MD, and Kumar G. Belani, MBBS MS^*

Departments of *Anesthesiology, Obstetrics and Gynecology, and Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota; and Department of Anesthesiology, University of California Medical School, San Francisco, California

Address correspondence and reprint requests to David S. Beebe, MD, Professor, Department of Anesthesiology, University of Minnesota Medical School, MMC 294, B515 Mayo Memorial Building, 420 Delaware St. S.E., Minneapolis, MN 55435. Address e-mail to beebe001{at}tc.umn.edu

	Abstract

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We conducted this study to investigate the effect of insufflation pressure on the pathophysiology of CO₂ pneumoperitoneum and embolism in an infant model. Twenty anesthetized piglets had stepwise intraperitoneal insufflation with CO₂ for 15 min at pressures ranging from 5 to 20 mm Hg. The piglets were ventilated to baseline normocarbia (ETCO₂ = 30 mm Hg, PaCO₂ = 38 mm Hg) before beginning each insufflation. CO₂ was then insufflated IV in 15 of these piglets at the same pressures. There was no reduction of blood pressure or cardiac output with intraperitoneal insufflation, but the stroke volume declined significantly (*P < 0.05) from (mean ± SE) 10.6 ± 1.3 mL to 8.5 ± 1.3* mL and from 10.0 ± 1.4 mL to 7.2 ± 1.2* mL at 15 and 20 mm Hg insufflation pressure, respectively. Abdominal insufflation at 5, 10, 15, and 20 mm Hg caused an increase in ETCO₂ to 31.7 ± 0.8 mm Hg, 35.6 ± 1.2* mm Hg, 37.5 ± 1.5* mm Hg, and 40.1 ± 1.8* mm Hg and in PaCO₂ to 41.1 ± 1.3* mm Hg, 44.2 ± 1.4* mm Hg, 49.9 ± 1.8* mm Hg, and 53.0 ± 2.1* mm Hg, respectively. In contrast, the ETCO₂decreased to 19.4 ± 1.5* mm Hg, 20.4 ± 1.4 mm Hg, 15.2 ± 2.1* mm Hg, and 10.6 ± 2.0* mm Hg with IV insufflation using the same pressures. IV insufflation caused marked hypotension and mortality. As the insufflation pressure increased, the mortality increased (0 in 15, 1 in 15, 1 in 14, and 6 in 13* at 5, 10, 15, and 20 mm Hg; *P < 0.05 vs 0 in 15, 1 in 15, and 1 in 14). This study suggests that although intraperitoneal insufflation up to 20 mm Hg may be tolerated hemodynamically, the lowest possible pressure should be used to reduce hypercarbia. A low insufflation pressure may also prevent mortality from CO₂ embolism.

IMPLICATIONS: The lowest pressure possible should be used when inflating the abdomen with CO₂ to perform a laparoscopy in babies. A low pressure allows better ventilation and may prevent mortality if CO₂ is accidentally injected into a vein.

	Introduction

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Laparoscopic surgery is becoming common in pediatric patients. Pediatric anesthesiologists must now manage the complications associated with laparoscopy. Most children tolerate abdominal insufflation and laparoscopic surgery with few perioperative problems (1). Hypercarbia, hypoxia, and hyper- and hypotension have been reported during laparoscopy in infants and young children, however (2).

An additional complication that is unique to laparoscopic surgery is CO₂ embolism. A CO₂ embolism can occur if the insufflating needle or catheter is accidentally placed into a vein, artery, or vascular organ such as the uterus. This potentially catastrophic complication has been extremely rare (15 per 113,253 cases in gynecological laparoscopy) (3). However, the incidence may be increasing as laparoscopy is being performed on patients with previous abdominal operations and dense adhesions (4). The hemodynamic and metabolic effects of abdominal insufflation have been studied at length, both clinically in adult humans and in animal models (5). The effect of insufflation pressure on the physiology and mortality from CO₂ embolism has also been studied experimentally in adult animals (6). However, little has been written about the effects of insufflation pressure during pneumoperitoneum or CO₂ embolism in babies. In this study, the piglet was chosen as an infant animal model because of the similarity of its cardiovascular system to that of humans (7). We hypothesized that increasing the insufflation pressure would result in hemodynamic instability during pneumoperitoneum and increased mortality with CO₂ embolism. The aim of this study was to determine the cardiopulmonary effects and mortality of CO₂ pneumoperitoneum and embolism in piglets at insufflation pressures varying from 5 to 20 mm Hg.

	Methods

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After approval by the University of Minnesota Animal Care and Use committee, 20 piglets, 4 to 6 wk old, weighing (mean ± SE) 8.2 ± 0.5 kg (range, 3.4–11.8 kg) were premedicated with IM Telazol (tiletamine and zolazepam) (Fort Dodge Animal Health, Fort Dodge, IA) 10 mg/kg and atropine 0.1 mg/kg. The animals were fasted the night before the operation. The trachea of each piglet was intubated with a 5.0 cuffed endotracheal tube, and anesthesia was maintained with 1% isoflurane. Neuromuscular blockade was provided with intermittent IV doses of vecuronium or pancuronium. Ventilation was provided with a Servo 900 C ventilator (Siemens-Elema AB, Solna, Sweden) by using an air/oxygen mixture with a fraction of inspired oxygen of 50%, initially set to deliver a tidal volume of 10 mL/kg. The respiratory rate was adjusted to maintain the PaCO₂ between 35 and 40 mm Hg. Low-compliance tubing (1 mL/cm H₂O pressure; Simplex Medical Systems Inc., Las Vegas, NV) was used for the breathing circuit. The peak airway pressure (P_aw) was measured each breath by the ventilator. Bladder and oral/gastric catheters were also placed. Forced-air surface warming (Bair Hugger^®; Augustine Medical Inc., Eden Prairie, MN) was used to maintain the core temperature at >37°C. All piglets received an initial IV fluid bolus of 10 mL/kg of normal saline, followed by an infusion of 4 mL · kg^-1 · h^-1 of the same solution. The electrocardiogram and arterial oxygen saturation were monitored continuously throughout the study. ETCO₂ was monitored continuously with a Nellcor N-1000/N-2500 (Nellcor Inc., Pleasanton, CA) gas analyzer with airway gas sampling set at 150 mL/min (delay time, 1755 ms; dynamic response of cuvette, 17 ms; total response time, 1932 ms). The femoral artery and vein, as well as the right internal jugular vein, were cannulated to determine the mean arterial blood pressure, femoral venous pressure (FVP), and central venous pressure (CVP), respectively. The contralateral femoral vein was cannulated as well with a 16-gauge Teflon catheter. The catheter was advanced 13 cm up the femoral vein into the vena cava. This catheter was used for intravascular insufflation. A precordial Doppler device (Versatone^®; Medasonics, Mountain View, CA) was used to detect the presence of gas embolism. The precordial Doppler device can detect venous gas embolism at levels as low as 0.05 mL/kg (8). The Doppler probe was placed on the midsternal region of each pig. Proper placement and functioning of the precordial probe was confirmed by noting changes in the Doppler sound pattern after the rapid intravascular injection with 10 mL of agitated IV fluid. In 10 piglets, transesophageal echocardiography with a pediatric biplane esophageal probe (Hewlett-Packard, Andover, MA) was used to determine the cardiac output during abdominal insufflation. The mean arterial blood pressure, FVP, CVP, electrocardiogram, and ETCO₂ were monitored and recorded every 10 s by using the labVIEW program (National Instruments, Austin, TX) throughout the experiment.

After placement of invasive monitors and a 30-min stabilization period, a Veress insufflation needle was placed via a small incision into the peritoneal cavity. Intraperitoneal insufflation was performed in a stepwise fashion from 5 to 20 mm Hg in 5 mm Hg increments by using a Karl Storz insufflator (Karl Storz Co., Culver City, CA) in the first 10 piglets. The insufflation rate was set at 0.6 L/min. The total volume of gas insufflated was measured and recorded by the Karl Storz insufflator. The baseline minute volume ventilation was not altered during insufflation. The abdomen was insufflated for 15 min for each pressure, followed by a 30-min recovery period. In the second 10 piglets, the same insufflation pressures were used, but the sequence was randomized to determine whether the measured variables were affected by the order of insufflation in the first 10 pigs. Arterial blood gases and electrolytes were determined 1 min before the beginning and 1 min before the end of insufflation at each pressure by use of an IL 1400 BGElectrolytes Analyzer (Instrumentation Laboratory, Lexington, MA).

After completion of the intraperitoneal portion of the experiment and a 45-min stabilization period, IV insufflation was begun. In 15 animals IV insufflation was performed in a stepwise manner, with increasing insufflation pressures beginning at 5 mm Hg pressure at the same insufflation rate (0.6 L/min) as the intraperitoneal injection. The injection lasted either for 5 min or until the ETCO₂ decreased to <50% of baseline, at which time it was halted in an effort to save the animal. Arterial blood gases and electrolytes were determined 1 min before the beginning of intravascular insufflation and immediately after ending insufflation. There was a 45-min recovery period before intravascular insufflation at the next pressure was begun.

The number of animals in which the insufflation had to be stopped before 5 min was recorded for each insufflation pressure, and the number of animals that died was noted. If a piglet survived insufflation to 20 mm Hg pressure, intravascular injection was performed at 25 mm Hg until death occurred.

In the remaining four animals, intravascular injections were begun at higher initial pressures. This was done to determine whether mortality would still occur without prior intravascular insufflation at lower pressures. Two pigs had intravascular insufflation begun at 10 mm Hg, one animal at 15 mm Hg, and one at 20 mm Hg pressure. The hemodynamic and metabolic data from these four piglets were not included in the analysis, and their mortality was reported separately.

Normally distributed data are presented as mean ± SE. Categorical data and data not normally distributed were reported either as the absolute value or the median value and the range. Categorical data were compared by using Fischer’s exact, Kruskal-Wallis, or Friedman’s tests. The hemodynamic and biochemical data for the intraperitoneal insufflation were analyzed with analysis of variance (ANOVA) for repeated measures comparing the ordered and nonordered groups of pigs, as well as the effect of insufflation pressure. If there was a significant effect of insufflation pressure on a measured variable, the effects of each pressure were compared with baseline and with each other by using Scheffé tests. The hemodynamic and biochemical data from the pigs that survived stepwise IV insufflation from 5 to 20 mm Hg were also analyzed with ANOVA for repeated measures followed by Scheffé tests. Significance was defined as P < 0.05.

	Results

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There were no significant differences between the effects of insufflation pressure between the ordered and nonordered groups of pigs in any of the variables measured during intraperitoneal insufflation. Therefore, the combined data for both the ordered and randomized groups of pigs were reported. The total volume of CO₂ insufflated intraperitoneally was 0.6 ± 0.1 L at 5 mm Hg, 1.1 ± 0.1 L at 10 mm Hg (P < 0.001 vs 5 mm Hg), 1.3 ± 0.1 L at 15 mm Hg (P < 0.001 vs 5 mm Hg, P = not significant versus 10 mm Hg), and 1.7 ± 0.1 L at 20 mm Hg (P < 0.001 vs 5 and 10 mm Hg, P < 0.01 vs 15 mm Hg).

There were stepwise increases in the ETCO₂, PaCO₂, and P_aw with increasing insufflation pressures (Figs. 1 and 2). The PaO₂ declined with increasing insufflation pressure (Fig. 2), but there were no changes in oxygen saturation measured by pulse oximetry from the initial value (median value, 100%; range, 98%–100%). Intraperitoneal insufflation to 20 mm Hg resulted in minimal change in the systemic hemodynamics other than a decline in stroke volume at 15 and 20 mm Hg pressure (Fig. 3). The FVP and CVP increased directly with the insufflation pressure. However, the increase in FVP was markedly greater at all pressures than the increase in the CVP. For example, the FVP increased from 7.5 ± 0.5 mm Hg to 24.7 ± 0.8 mm Hg (P < 0.0001) with insufflation to 20 mm Hg. In contrast, the CVP increased only from 5.0 ± 0.5 mm Hg to 9.5 ± 1.4 mm Hg (P < 0.0001) with insufflation to the same pressure.

View larger version (41K): [in this window] [in a new window]   Figure 1. ETCO2 and PaCO2 versus insufflation pressure for 20 piglets receiving intraperitoneal insufflation and 15 of the same piglets receiving IV insufflation. One piglet died after IV insufflation at 10 mm Hg, one after insufflation at 15 mm Hg, and six after insufflation at 20 mm Hg pressure. Both intraperitoneal and IV insufflation had significant (P < 0.0001) effects on the ETCO2 and PaCO2. *P < 0.05 versus baseline; **P < 0.05 versus baseline and 5 mm Hg; ¥P < 0.05 versus baseline and 5 and 10 mm Hg.

View larger version (50K): [in this window] [in a new window]   Figure 2. PaO2 and peak airway pressure (Paw) versus insufflation pressure for intraperitoneal and IV insufflation. Significant (P < 0.0001) effects of intraperitoneal insufflation were noted for both the PaO2 and Paw. The PaO2 was also affected significantly (P < 0.0001) by IV insufflation, but the Paw was not. *P < 0.05 versus baseline; **P < 0.05 versus baseline and 5 mm Hg; ¥P < 0.05 versus baseline and 5 and 10 mm Hg; P < 0.05 versus baseline and 5, 10, and 15 mm Hg.

View larger version (20K): [in this window] [in a new window]   Figure 3. Cardiac output, systemic vascular resistance (SVR), and stroke volume versus insufflation pressure for intraperitoneal insufflation. There was a significant (P < 0.05) effect of insufflation pressure on stroke volume. *P < 0.05 versus baseline.

The ETCO₂ decreased markedly with increasing pressure with intravascular insufflation, although the PaCO₂ increased (Fig. 1). The P_aw did not change with intravascular injection, but the PaO₂ decreased markedly as the insufflation pressure was increased (Fig. 2). The arterial oxygen saturation measured by pulse oximetry did not change from the baseline median value of 100% (range, 99%–100%) with IV insufflation at 5 mm Hg (range, 89%–100%) or 10 mm Hg (range, 0%–100%), but it declined significantly (P < 0.001) from 100% to 0% in all piglets insufflated to 15 mm Hg (range, 0%–98%) and 20 mm Hg (range, 0%–100%).

Most piglets (11 of 15) received the full 5 min of intravascular insufflation at 5 mm Hg pressure. In the remainder, the injection was halted before 5 min because the ETCO₂ decreased to <50% of the control values. Similarly, the majority of pigs (9 of 15) tolerated intravascular insufflation at 10 mm Hg pressure. In contrast, only one piglet tolerated insufflation at 15 mm Hg for 5 min (1 of 14; P < 0.001 vs 5 mm Hg; P < 0.01 vs 10 mm Hg), and only one piglet tolerated insufflation at 20 mm Hg (1 of 13; P < 0.001 vs 5 mm Hg; P < 0.01 vs 10 mm Hg).

Despite stopping insufflation if the ETCO₂ decreased to <50% of the control value, mortality often occurred. Death was always preceded by profound hypotension. In most cases (16 of 19), bradycardia and then asystole followed the hypotension. One pig developed complete heart block as well as profound hypotension after intravascular insufflation, and two piglets initially had tachycardia (>200 bpm) after insufflation before developing bradycardia and asystole. Death occurred more frequently as the insufflation pressure increased (0 of 15, 1 of 15, 1 of 14, and 6 of 13 at 5, 10, 15, and 20 mm Hg pressure, respectively). More piglets died when insufflated intravascularly to 20 mm Hg than at any of the lower pressures (P < 0.05 vs 5, 10, or 15 mm Hg). Insufflation to 25 mm Hg in the seven surviving animals resulted in mortality in 3.2 ± 1.2 min (range, 0.1–8 min). In the two pigs in which stepwise insufflation was begun at 10 mm Hg, mortality occurred after insufflation at 20 and 25 mm Hg, respectively. Both pigs with insufflation begun at 15 and 20 mm Hg died after insufflation at these pressures.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
Although laparoscopic surgical instruments and trocars are being developed for small pediatric patients, the same mechanical insufflators are used as for adults. The surgeon selects the pressure desired in the abdomen for surgical exposure as well as the maximal flow rate for insufflation. During the beginning of insufflation, CO₂ is initially injected at the maximal flow rate. The machine periodically stops insufflation and measures the intraperitoneal pressure. For example, the Karl Storz insufflator used in this study injects CO₂ for 1.7 seconds and then measures the pressure for 15 minutes. The machine automatically reduces the flow rate as it senses pressure building up in the abdomen, and then it halts it at the set pressure (Karl Storz Co., personal communication, 1998). Pediatric surgeons select a slow maximal flow rate (0.6 L/min) because the volume needed to be insufflated is small. A slow flow rate also reduces the severity of a CO₂ embolism if inadvertent intravascular injection occurs.

Surgeons often use an insufflation pressure between 10 and 14 mm Hg to perform laparoscopy in older children or adults. Lower insufflation pressures have been suggested for babies or small children. For example, Sfez (9) recommended that an insufflation pressure no higher than 6 mm Hg be used for laparoscopy on infants younger than six months old. He believed that insufflation to higher pressures carried the risk of low cardiac output because of the reduced myocardial compliance and contractility in this age group. In our experiment, piglets tolerated abdominal insufflation to 20 mm Hg without reduction in blood pressure or cardiac output. These results were similar to those of an earlier piglet study in which the cardiac output was measured directly with ultrasonic flowprobes placed around the ascending aorta. In that experiment, the cardiac output did not decline with insufflation to 15 mm Hg (10).

Several studies in infants have demonstrated a moderate decline in cardiac index (10%–30%) by using transesophageal Doppler imaging to measure the flow in the descending aorta (11,12). However, blood flow in the abdominal aorta may not reflect the cardiac output if insufflation causes redistribution of circulation to the upper body (13). A recent study with transthoracic echocardiography that measured the cardiac output in the ascending aorta demonstrated no decrease in cardiac index during insufflation to 15 mm Hg pressure in infants (14). Another study with transesophageal echocardiography in children two to six years old demonstrated no diminution in cardiac index with insufflation to 6 mm Hg and demonstrated a small decline (13%) with insufflation to 12 mm Hg (13).

Our study suggested that low insufflation pressures may still be beneficial in infants or small children, however. Low insufflation pressures 1) help to prevent or control hypercarbia associated with CO₂ insufflation, 2) allow better ventilation with improved oxygenation, 3) limit the increase of peripheral venous pressures associated with abdominal insufflation, and 4) reduce the risk of mortality from accidental CO₂ embolism. In this experiment, abdominal insufflation caused a stepwise increase in the P_aw with increasing insufflation pressure. High airway pressures result in loss of tidal volume from compressibility of gases in the system and expansion of the ventilator tubing. This can result in hypoventilation and hypercarbia if appropriate adjustments are not made. Volume loss in standard anesthesia machine ventilators can be as high as 6 to 12 mL/cm H₂O airway pressure (15). In addition, the PaO₂ in the piglets declined as the insufflation pressure increased. This was probably due in part to the reduction in ventilation at higher insufflation pressures. Abdominal insufflation also limits the excursion of the diaphragm and reduces the functional residual capacity. The reduction in functional residual capacity may be greater at higher insufflation pressures and may result in atelectasis and hypoxia (16).

Although the cardiac output was maintained, the FVP became markedly increased in the piglets as the insufflation pressure increased. This increase in FVP and the stepwise increase in the pressure gradient between the FVP and CVP have been demonstrated previously in adult humans (17). Blood accumulates in the veins of the lower extremities until the venous pressure becomes high enough to overcome the resistance in the vena cava caused by abdominal insufflation. A low insufflation pressure may benefit an infant with hypovolemia who cannot tolerate volume loss from this sequestration of blood (18).

Using a low insufflation pressure may also be life-saving if CO₂ is accidentally injected into the vascular system. In a previous experiment with older, larger pigs, the volume of CO₂ injected intravascularly was twice as much at 20 mm Hg insufflation pressure (16.7 ± 3.9 mL/kg) than at 15 mm Hg (8.3 ± 2.7 mL/kg). Most (80%) of the pigs in that experiment died when insufflated at 20 mm Hg, but all survived if lower pressures were used (6). In our study, the volume of CO₂ injected was so small that the amount could not be recorded by the insufflator, even if it proved lethal. However, as in the larger animals, the mortality increased markedly as the insufflation pressure increased to >15 mm Hg.

The ETCO₂ always decreased with IV insufflation in piglets. In contrast, in the earlier experiment with older pigs and in some case reports of CO₂ embolism in humans, the ETCO₂ initially increased. In both the animal experiment and the case reports, the ETCO₂ then rapidly declined as the embolism progressed (6,19).

Small quantities of CO₂ injected intravascularly dissolve and increase the CO₂ content of the blood, thus increasing the ETCO₂. As the volume of gas injected increases, CO₂ blocks blood flow in the pulmonary arterioles. A decrease in ETCO₂ occurs as areas of the lung are ventilated but not perfused (6). Perhaps less CO₂ could be dissolved in the small blood volume of a piglet compared with the rate of insufflation. The pulmonary vasculature is also more responsive to acidosis, hypercarbia, and hypoxia in a baby animal (20). Large concentrations of CO₂ may have produced pulmonary vasoconstriction and caused a decline in ETCO₂.

In summary, piglets tolerated insufflation to 20 mm Hg without hemodynamic compromise. However, hypercarbia developed at higher insufflation pressures, and ventilation and oxygenation became more difficult. The mortality from IV insufflation was also increased as the insufflation pressure increased. This study suggests that low insufflation pressures should be used when performing laparoscopic surgery in infants and small children.

	Acknowledgments

 
Supported by a grant from the Minnesota Medical Foundation.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Beebe, D. S. Articles by Belani, K. G. Search for Related Content PubMed PubMed Citation Articles by Beebe, D. S. Articles by Belani, K. G.