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PEDIATRIC ANESTHESIA

Preserved CO₂ Reactivity and Increase in Middle Cerebral Arterial Blood Flow Velocity During Laparoscopic Surgery in Children

Egbert Huettemann, MD, DEAA^*, Christoph Terborg, MD, Samir G. Sakka, MD^*, Gritta Petrat, MD^*, Felix Schier, MD, PhD, and Konrad Reinhart, MD, PhD^*

Departments of *Anesthesiology and Intensive Care Medicine, Neurology, and Pediatric Surgery, Friedrich-Schiller-University Jena, Jena, Germany

Address correspondence and reprint requests to Egbert Hüttemann, MD, DEAA, Klinik für Anästhesiologie und Intensivtherapie, Friedrich-Schiller-Universität Jena, Bachstrasse 18, D-07740 Jena, Germany. Address e-mail to Egbert.Huettemann{at}med.uni-jena.de

	Abstract

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In adult patients, the creation of pneumoperitoneum (PP) by means of carbon dioxide (CO₂) insufflation leads to an increase in cerebral blood flow velocity (CBFV), which is thought to be caused by hypercapnia. We evaluated whether PP leads to an increase of CBFV in children, and whether this increase is directly related to PP. The effects of PP on middle cerebral artery blood flow velocity were investigated in 12 children (mean age 3 yr, range 15–63 mo) undergoing laparoscopic herniorrhaphy under general anesthesia with sevoflurane and nitrous oxide/oxygen. CBFV was measured by using transcranial Doppler ultrasonography. During CO₂ insufflation, the end-tidal CO₂ concentration was kept constant by adjustment of ventilation by increasing minute volume. The CBFV increased significantly at an intraabdominal pressure of 12 mm Hg compared with baseline from 68 ± 11 cm/s to 81 ± 12 cm/s (P < 0.05). CO₂ reactivity remained in the normal range (4.0% ± 1.9%/mm Hg) during PP. We conclude that the induction of PP leads to an increase in middle cerebral artery blood flow velocity in young children independent from hypercapnia, whereas CO₂ reactivity remains normal.

IMPLICATIONS: Laparoscopic surgery is performed frequently in pediatric patients. Cerebral blood flow velocities increase during insufflation of the intraperitoneal cavity for minimally invasive surgery in children. The vasoreactivity as part of the cerebral autoregulation remains unaffected.

	Introduction

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As in adult surgery, laparoscopic techniques have become standard procedures in pediatric surgery. An investigation in adult patients has shown that carbon dioxide (CO₂) leads to an increase in middle cerebral blood flow velocity (CBFV), which is thought to be caused by hypercapnia (1). No data exist on pediatric patients, particularly whether pneumoperitoneum (PP) per se leads to an increase in CBFV independent from end-tidal CO₂ concentration (PETCO₂) and whether CBFV-CO₂ reactivity remains normal. Our hypothesis was that CBFV does not increase during PP if PETCO₂ is held constant during the procedure and that CBFV-CO₂ reactivity will remain in the normal range. To study the effect of PP on CBFV and CO₂-induced vasomotor reactivity under general inhaled anesthesia, we conducted a prospective study in pediatric patients undergoing laparoscopic herniorrhaphy.

	Methods

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After approval by the institutional ethics committee and informed parental consent, 12 patients (6 boys and 6 girls) undergoing laparoscopic herniorrhaphy were studied. The infants were between 15 and 63 mo of age (mean 35 mo), mean weight 15 kg (SD 5 kg), and were ASA physical status I. None of the children had cardiovascular, respiratory, or cerebrovascular disease, or were receiving medication.

All children received a standardized anesthetic. After premedication with midazolam (0.5 mg/kg) per os, anesthesia was induced with thiopental (5 mg/kg), and fentanyl (0.3 µg/kg), and maintained with 0.75 minimum alveolar anesthetic concentration (MAC) of sevoflurane and 67% nitrous oxide in oxygen (2). Intubation was facilitated by rocuronium (0.6 mg/kg). Mechanical ventilation was performed using a pressure-controlled mode (AS3; Datex-Engstroem, Helsinki, Finland) in which I/E ratio was 1:1 and end-expiratory pressure was maintained at 5 cm H₂O throughout the procedure. Controlled ventilation was adjusted before CO₂ insufflation to keep PETCO₂ at 34 mm Hg. After CO₂ insufflation, ventilatory frequency was increased to maintain a constant PETCO₂. Later, PETCO₂ was allowed to increase to a level of 38 mm Hg to allow calculation of the CO₂ vasoreactivity. After deflation of the abdomen, ventilatory frequency was reduced to preinsufflation levels.

Noninvasive systolic, diastolic, and mean arterial blood pressure (MAP), heart rate (HR), peripheral oxygen saturation, fraction of inspired oxygen, PETCO₂, body temperature, respiratory minute volume, airway pressures, and inspiratory and end-tidal concentrations of nitrous oxide and sevoflurane were continuously monitored throughout the study (AS3; Datex). Because I/E ratio was 1:1, airway pressure (Pmean) was calculated as: Pmean = positive end-expiratory pressure + inspiratory plateau pressure/2.

Blood flow velocity in the middle cerebral artery (MCA) was measured by using a transcranial ultrasonography probe (Multidop T; DWL Medizintechnik, Sipplingen, Germany). The probe was positioned over the temporal bone window (the temporal area just above the zygomatic arch) and was fixed to the patient’s head with an elastic bandage so that the angle of insonation remained constant during the investigation. Doppler signals from the MCA, M1 segment, were identified and measured at a depth of 30–40 mm. Time-averaged MCA blood flow velocity was calculated and monitored continuously. Blood flow velocities were expressed in centimeter/second. The pulsatility index (PI), an index reflecting waveform appearance, was calculated according to the formula PI = (systolic velocity - diastolic velocity)/mean velocity.

After stabilization of respiratory and hemodynamic variables, defined as changes in MAP, HR, PETCO₂, and expiratory anesthesia gas concentrations of <10% within 10 min, the blood flow velocity in the MCA was measured after the induction (baseline), and after the insufflation of the abdominal cavity with CO₂ at an intraabdominal pressure (IAP) of 12 mm Hg at 2 PETCO₂ levels, 34 mm Hg (PP₁ 12) and 38 mm Hg (PP₂ 12). The last measurements were obtained 10 min after abdominal deflation at the end of surgery while maintaining anesthesia unchanged (control).

All values were expressed as mean (SD). Statistical analysis was performed by using analysis of variance for repeated measurements and a pairwise multiple comparison procedure (Student-Newman-Keuls method, SigmaStat; SPSS, Chicago, IL). A probability of <0.05 was regarded as statistically significant.

	Results

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The results are summarized in Table 1. Significant hemodynamic changes included an increase in MAP (P < 0.05) after CO₂ insufflation into the abdominal cavity compared with baseline. After deflation of the peritoneal cavity, MAP returned to baseline values. CBFV during PP at an IAP of 12 increased significantly compared with baseline (v_mean MCA: 68 ± 11 cm/s to 81 ± 12 cm/s) (P < 0.05) and decreased to baseline values 10 min after peritoneal desufflation (Table 1). After the induction of PP, PI decreased significantly from 1.1 ± 0.2 to 0.8 ± 0.2 (P < 0.05). The CO₂ reactivity, calculated by means of CBFV at two levels of PETCO₂ (34 and 38 mm Hg), was 4.0% ± 1.9%/mm Hg change in PETCO₂. The mean airway pressure increased from 14 ± 3 mm Hg to 16 ± 4 mm Hg.

	Discussion

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Cerebral blood flow (CBF) can be measured by several techniques. Transcranial Doppler ultrasound is a safe, noninvasive method, thus rendering it particularly useful in children. Although CBF cannot be absolutely quantified with this method, a comparison with PET measurements revealed a close correlation between changes in CBF and changes in CBFV during vasomotor reactivity tests (3,4). Consequently, transcranial Doppler sonography is a useful tool in studying hemodynamic changes, e.g., during surgical procedures.

Blood pressure, cardiac output (CO), body temperature, intrathoracic pressure, and depth of anesthesia may influence CBF (5). In the present investigation, temperature remained constant during the study. There was a slight, but not significant, increase in mean airway pressure, likely reflecting an increase in intrathoracic pressure. Whereas halothane tends to increase CBF (6), neither isoflurane nor sevoflurane (0.5–1.5 MAC) produce significant dose-related changes of blood flow velocities (7). Furthermore, CBF autoregulation remains intact during 0.5 and 1.5 MAC sevoflurane anesthesia (8). In this study, the end-tidal concentration of sevoflurane was kept constant at 0.75 MAC. Nitrous oxide causes a mild increase in CBFV (9,10) but it does not affect the dynamic cerebrovascular reactivity in acute arterial CO₂ changes (9,10). Thus, because the anesthetic concentrations remained constant throughout the study period, our results cannot be explained by cerebral vasodilation caused by anesthetics or by impaired autoregulation.

Our finding of an increased CBFV during PP indicates either an increase in CBF or a constriction of the insonated vessel. CBF remains constant if cerebral perfusion pressure is varied between 60 and 130 mm Hg of MAP (11). However, the increase in MAP occurring in the setting during PP is mediated by catecholamines and vasopressin (12–15). Several investigations have demonstrated that norepinephrine may lead to significant increases in CBFV (16–18). Indirect evidence for vasopressor (norepinephrine and/or vasopressin) related MCA vasoconstriction is provided by the decrease in PI. Investigators studying the hemodynamic effects of PP in infants reported a decrease in cardiac index after insufflation. In one study using noninvasive continuous esophageal aortic blood flow echo-Doppler, a decrease in aortic blood flow and stroke index of 33% and 32%, respectively, has been described at an IAP of 10 mm Hg (19). Another study using transesophageal echocardiography found a decrease in cardiac index and stroke index of 13% and 5%, respectively, at an IAP of 12 mm Hg (20). Given these data, there is no evidence that the increase in CBFV during PP is related to an increase in stroke volume or CO. However, we cannot exclude a redistribution of CO during PP leading to an increase in CBF.

In an investigation of adult patients undergoing laparoscopic cholecystectomy, CO₂ insufflation up to an IAP of 10 mm Hg was shown to lead to an increase of CBFV of approximately 30% (1). Ventilation was kept constant and arterial CO₂ concentration (PaCO₂) increased from 36 to 39 mm Hg. However, this increase in PaCO₂ does not fully explain the observed increase of CBFV. Given the CO₂ vasoreactivity of 3%–4% per mm Hg change in PaCO₂ measured in that study, an increase in PETCO₂ of 3 mm Hg would only account for an increase of approximately 9% in the CBFV (about one-third of the total 30% increase). Thus, approximately 60%–70% of the increase in CBFV was directly related to the PP and not to hypercapnia. Thus, an additional cause for the increase in CBFV is supported by data in adults as well.

Because PaCO₂ profoundly influences CBF and hypercapnia causes intense cerebral vasodilation and increases CBF (8), PETCO₂ was kept constant by adjustment of minute volume. We did not routinely measure PaCO₂ because this would have required placement of an arterial line. Data from adult studies indicate that the difference between PaCO₂ and PETCO₂ (alveolo-arterial gradient) remains constant during the creation of a PP in adults over a wide range of values (21–23). In two cases (two and three years of age) independent of this study, in which the PaCO₂ was measured, the alveolo-arterial gradient did not change. If a change of the alveolo-arterial gradient is to occur during a PP, one might at the earliest expect an increase of the alveolo-arterial gradient. Given a constant PETCO₂, this would lead to an underestimation of the increase of CBFV, because a decrease in PaCO₂ would, in part, counteract the PP-induced increase in CBFV. Thus, the increase in CBFV cannot be explained by an increase in PaCO₂.

An important finding of this study is the preserved CO₂ reactivity during PP. The CO₂ reactivity slope (relative change of CBFV in relation to a defined change of PETCO₂) value of 4.0% ± 1.9%/mm Hg in this study was almost in the same range as that described for the awake state (3.2%) (24).

There are two major limitations of our study. First, we did not determine baseline CBFV-CO₂ reactivity to compare with CBFV-CO₂ reactivity during PP. Thus, it remains open whether CBFV-CO₂ reactivity, though being in the normal range, is altered during PP. Second, we did not investigate CBFV-CO₂ reactivity to hypocapnia in order to evaluate that hyperventilation could overcome the effects of PP on CBFV. These issues need to be studied.

In summary, the major findings of this study are that the induction of PP leads to an increase in MCA blood flow velocity in young children independent from changes in PETCO₂, and that CO₂ reactivity is preserved.

	Footnotes

 
Presented in part at the ASA annual meeting, Dallas, TX, October 10–13, 1999.

	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 (4) Citing Articles via Google Scholar Google Scholar Articles by Huettemann, E. Articles by Reinhart, K. Search for Related Content PubMed PubMed Citation Articles by Huettemann, E. Articles by Reinhart, K. Related Collections Monitoring (Non-cardiac) Pediatrics