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REGIONAL ANESTHESIA

Perioperative Glucose Infusion and the Catabolic Response to Surgery: The Effect of Epidural Block

Ralph Lattermann, MD^*, Franco Carli, MD, MPhil^*, Linda Wykes, PhD, and Thomas Schricker, MD, PhD^*

*Department of Anesthesia and School of Dietetics and Human Nutrition, McGill University, Montreal, Quebec, Canada

Address correspondence and reprint requests to Franco Carli, MD, Department of Anesthesia, McGill University, Royal Victoria Hospital, Room S9.16, 687 Pine Ave. West, Montreal, Quebec, Canada H3A 1A1. Address e-mail to franco.carli{at}mcgill.ca

	Abstract

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Although the nitrogen-sparing properties of epidural block and IV glucose on the days after surgical trauma have been well established, their metabolic effects during the acute phase of the stress response remain unclear. Therefore, in this study we investigated the effect of epidural block on glucose and protein kinetics during and immediately after surgery in patients receiving IV glucose at 2 mg · kg^-1 · min^-1. Sixteen patients undergoing colorectal surgery received either general anesthesia with epidural block with bupivacaine (EDA; n = 8) or general anesthesia alone (control; n = 8). Glucose and protein kinetics were determined during and 2 h after the operation by stable isotope tracers [6,6-²H₂]glucose and L-[1-¹³C]leucine. Plasma concentrations of glucose, insulin, cortisol, and glucagon were also determined. Epidural block attenuated the perioperative increase in plasma glucose concentration (P < 0.05). The rate of appearance of glucose (R_a glucose) and endogenous glucose production (EGP) were slower in the EDA group than in control subjects during (R_a glucose, EDA 13.2 ± 1.0 versus control 15.3 ± 1.8 µmol · kg^-1 · min^-1; P < 0.05; EGP, EDA 1.2 ± 1.2 versus control 3.8 ± 1.7 µmol · kg^-1 · min^-1; P < 0.05) and after the operation (P > 0.05). Whereas protein breakdown and amino acid oxidation decreased in both groups (P < 0.05), whole-body protein synthesis remained unchanged. Insulin levels increased with both anesthetic techniques (P < 0.05). Intraoperative plasma concentrations of cortisol and glucagon were smaller in the EDA group (P < 0.05). The intraoperative suppression of EGP by exogenous glucose was more pronounced in the presence of epidural block. However, epidural block failed to exert a protein-sparing effect during the acute phase of the stress response in patients receiving IV glucose.

IMPLICATIONS:We investigated the effect of epidural block on perioperative glucose and protein kinetics in patients receiving IV glucose infusion. Endogenous glucose production and plasma glucose concentration were smaller in the presence of epidural block. However, epidural block did not modify perioperative protein metabolism during the administration of IV glucose.

	Introduction

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Glucose exerts its anticatabolic action through the suppression of gluconeogenesis and a reduced need for gluconeogenic amino acids released from the muscle (1). Whereas the protein preserving properties of glucose administration after surgery are well established, its use during the acute phase of surgical tissue trauma has produced conflicting results (2–4). On one side, glucose infused at 3 mg · kg^-1 · min^-1 during gastrectomy decreased plasma concentrations of branched-chain amino acids (BCAA), indicating an inhibition of whole-body protein breakdown (3). However, IV glucose at the same dose did not affect plasma BCAA concentrations during cholecystectomy (2) and did not improve nitrogen balance in patients undergoing craniotomy (4). Although it was proposed that this discrepancy might be because of the different types of surgery studied (3), plasma amino acid concentrations and nitrogen excretion values represent only indirect variables of protein breakdown and amino acid oxidation.

In addition to its influence on protein metabolism, intraoperative glucose infusion typically leads to a significant increase in plasma glucose concentration. This raises a concern about metabolism because acute hyperglycemia is associated with several disadvantageous clinical effects (5–8). Neuraxial block with epidural local anesthetic inhibits the increase in plasma glucose concentration during abdominal surgery in fasting patients (9,10), mediated through the attenuation of endogenous glucose production (EGP) (11). Despite this suppressory effect on glucose production however, epidural block fails to modify protein catabolism in the absence of nutritional support (11).

Several studies investigated the influence of intraoperative glucose administration on protein metabolism, but few were controlled for the type of analgesia. In particular, two studies addressed the effect of epidural block on the catabolic response in patients receiving IV glucose. The findings of the first study showed that the combination of epidural analgesia and general anesthesia was accompanied by a smaller splanchnic glucose release when compared with the control group receiving general anesthesia alone (12). In the other study, epidural block was associated with larger amino acid plasma concentrations but did not modify splanchnic amino acid uptake, indicating no effect on the rate of de novo glucose synthesis from gluconeogenic amino acids (13). However, the measurement of splanchnic amino acid metabolism does not provide insight into the kinetics of whole-body protein metabolism, and therefore, the influence of epidural block and glucose administration on protein breakdown and amino acid oxidation remains undetermined.

The present study was designed to test the hypothesis that the suppression of EGP by IV glucose (2 mg · kg^-1 · min^-1) would be more pronounced in patients receiving combined epidural block with bupivacaine and general anesthesia (EDA group) than in those with general anesthesia alone (control group). A larger decrease in glucose production in the EDA group would lead to a more accentuated inhibition of protein breakdown and amino acid oxidation. To provide an integrated analysis of glucose and protein metabolism during and immediately after surgery, glucose production, glucose clearance, and whole-body protein breakdown, amino acid oxidation and protein synthesis were assessed by the stable isotope tracers [6,6-²H₂]glucose and L-[1-¹³C]leucine.

	Methods

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The study was approved by the Ethics Committee of the Montreal General Hospital. Sixteen patients undergoing elective colorectal surgery were admitted to the study, and written informed consent was obtained from all subjects. No patient was suffering from cardiac, hepatic, renal, or metabolic disorders or receiving any medication known to affect metabolism. None of the participants had developed more than 5% weight loss over the preceding 3 months or had a hemoglobin <10 g/dL.

Patients were randomly assigned to the EDA group or the control group. In the EDA group, an epidural catheter was inserted between T9-11 before the operation. Neuraxial block was established with 0.5% bupivacaine to achieve a bilateral sensory block from T4-S5 and maintained with intermittent boluses of bupivacaine 0.25%. General anesthesia in all patients was induced with 5 mg/kg of thiopentone and 1.5 µg/kg of fentanyl in the EDA group or 5 µg/kg of fentanyl in the control group, respectively. Endotracheal intubation was facilitated with 0.6 mg/kg of rocuronium, and patients’ lungs were ventilated with 30% oxygen in air to maintain normocapnia. It has to be noted that no nitrous oxide was used because it has the same molecular weight as ¹³CO₂ and thus would interfere with the isotope ratio measurement of expired ¹³CO₂. General anesthesia in the control group was maintained using desflurane at end-tidal concentrations as required to keep heart rate within 20% of preoperative values. In the EDA group, desflurane was administered at end-tidal concentrations of approximately 3 vol% to achieve tolerance of the endotracheal tube and to prevent awareness. Supplemental doses of rocuronium were applied as required for complete surgical muscle relaxation. Fluid was given as NaCl 0.9% solution at a rate of 10 mL · kg^-1 · h^-1 during surgery and 6 mL · kg^-1 · h^-1 thereafter. All patients were covered with a warming blanket during surgery to maintain normothermia. Patients in the control group received morphine IV for postoperative pain relief. In the EDA group, the epidural block was maintained throughout the study period with bupivacaine 0.25% as required to maintain adequate sensory block (T8-L3). Hemodynamic monitoring was performed using a three-lead electrocardiogram monitor and radial artery catheterization for continuous blood pressure measurement.

All subjects received a solution of crystallized beet dextrose (10% dextrose anhydrous; Avebe, Foxhol, Holland) infused at 2 mg · kg^-1 · min^-1 starting with the surgical incision. This dose of glucose was chosen because previous studies showed that intraoperative plasma glucose concentrations in metabolically healthy surgical patients infused with glucose at 3 mg · kg^-1 · min^-1 regularly exceeded 10 mmol/L, the physiological threshold for renal glucose excretion (2–4). The solution was prepared by the local pharmacy under sterile conditions and was tested for sterility, stability, and absence of pyrogens before IV infusion. Beet dextrose was chosen because of its small ¹³C content and therefore the lack of perturbation of ¹³CO₂ enrichment in expired air (14).

Plasma kinetics of leucine and glucose were determined before, during, and 2 h after surgery by stable isotope tracer technique using primed continuous infusions of [6,6-²H₂]glucose and L-[1-¹³C]leucine (Cambridge Isotope Laboratories, Cambridge, MA). Sterile solutions of the isotopes were prepared, as previously described, and were kept at 4°C until the administration (11).

All patients were studied on the day of surgery beginning between 7:00 AM and 8:00 AM after fasting or approximately 36 h. Because of preparation of the bowel as required for colorectal surgery, patients received only clear fluids until midnight the day before the operation. A catheter was placed in a superficial vein in the dorsum of the hand and kept patent with a slow saline 0.9% infusion. A superficial vein of the contralateral arm was cannulated to provide access for the infusion of [6,6 ²H₂]glucose and L-[1-¹³C]leucine. After warming the hand in a heated air box to obtain arterialization of venous blood, blood and expired air samples were taken to determine baseline enrichments. Thereafter, priming doses of NaH¹³CO₃ 1 µmol/kg, L-[1-¹³C]leucine 4 µmol/kg, and [6,6-²H₂]glucose 22 µmol/kg were administered, followed immediately by continuous infusions of [6,6-²H₂] glucose 0.22 µmol · kg^-1 · min^-1 and L-[1-¹³C]leucine 0.06 µmol · kg^-1 · min^-1, respectively. Isotope infusion was uninterrupted throughout the entire study period. Expired breath and arterialized blood samples for the determination of isotopic enrichments as well as for the measurement of metabolic substrates (glucose, lactate, and free fatty acids [FFA]) and hormones (insulin, glucagon, and cortisol) were collected according to Figure 1.

View larger version (24K): [in this window] [in a new window]   Figure 1. Study protocol. -[1-13C]KIC, -[1-13C]ketoisocaproate.

Whole-body oxygen consumption (O₂) and carbon dioxide production (CO₂) were measured by indirect calorimetry before and 2 h after surgery using the open system indirect calorimetry device Deltatrac Metabolic Monitor (Datex Instrumentarium, Helsinki, Finland). CO₂ was also measured during surgery (70 min after skin incision). The values of O₂, CO₂, and respiratory quotient represent an average of the data obtained over a period of 20 min on each occasion, with a coefficient of variation <10%.

Plasma glucose was derivatized to its pentaacetate compound, and the [6,6-²H₂]glucose enrichment was determined by gas chromatography-mass spectrometry using electron-impact ionization (11). Plasma -[1-¹³C]ketoisocaproate (-[1-¹³C]KIC) enrichment was analyzed by electron-impact selected-ion monitoring gas chromatography-mass spectrometry (15), except that t-butyldimethylsylyl rather than trimethylsylyl derivatives were used. Expired ¹³CO₂ enrichment for the calculation of leucine oxidation was determined by isotope ratio mass spectrometry (Analytical Precision AP2, 003, Manchester, United Kingdom).

Plasma glucose concentrations were measured with a glucose analyzer 2 (Beckman Instruments, Fullerton, CA) based on a glucose oxidase method. The plasma lactate assay was based on lactate oxidase using the synchron CX 7 system (Beckman Instruments). Circulating concentrations of FFA were quantified by means of an enzymatic assay (Boehringer Mannheim, Laval, Quebec, Canada). Cortisol, insulin, and glucagon plasma concentrations were measured by a double antibody radioimmunoassay (Amersham International, Amersham, Bucks, United Kingdom).

Under steady-state conditions, the rate of appearance (R_a) of unlabeled substrate in plasma can be derived from the plasma enrichment (atom percent excess [APE]) calculated by R_a = I x (APE_inf/APE_pl - 1), where APE_inf is the tracer enrichment in the infusate, APE_pl is the tracer enrichment in plasma at steady-state, and I is the infusion rate of the labeled tracer. The APE values used in this calculation represent the mean of the APE values determined during each isotopic plateau. Steady-state conditions were assumed when the coefficient of variation of the APE values at isotopic plateau was <5%.

In a steady-state, leucine flux is defined by the formula: Q = S + O = B + I, where S represents the rate of leucine uptake for protein synthesis, O is the rate of oxidation of leucine, B is the rate of leucine derived from endogenous protein breakdown, and I is the rate at which leucine is entering the free pool from dietary intake. Inspection of this equation indicates that when studies are conducted in the postabsorptive state, flux is equal to breakdown (16). Plasma -[1-¹³C]KIC enrichment was used for calculating both flux and oxidation of leucine. The steady-state reciprocal pool model represents the intracellular precursor pool enrichment more precisely than leucine itself (17). In the calculation of leucine oxidation, correction factors of 0.76 for the fasting state and 0.81 for the fed state were used to account for the fraction of ¹³CO₂ released from ¹³C-labeled leucine oxidation but retained within slow turnover rate pools of the body (16,18).

In the fasted state, R_a glucose equals the rate of EGP. During glucose infusion, EGP was calculated by subtracting the glucose infusion rate from the total R_a glucose. The glucose clearance rate, an indicator of the tissues ability to take up glucose, was calculated as the R_a glucose divided by the corresponding glucose plasma concentration.

For metabolic substrates, hormones and hemodynamic variables, the average of the 2 intraoperative measurements at 60 and 100 min after skin incision was calculated and is presented in the tables.

Differences between the groups were analyzed using the Mann-Whitney U-test. Within-group comparison of variables was made by analysis of variance for repeated measures with post hoc analysis by Student-Newman-Keuls test. A probability of P < 0.05 was considered to be significant. Data are presented as mean ± SD.

	Results

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There were no differences between the two groups regarding age, height, weight, sex, and the American Society of Anesthesiologists classification (Table 1). The duration of surgery, estimated blood loss, and the amount of crystalloid fluid administered were comparable in both groups.

View larger version (23K): [in this window] [in a new window]   Figure 2. Isotopic enrichments (atom percent excess [APE]) of [6,6-2H2]glucose, -[1-13C]ketoisocaproate (-[1-13C]KIC), and 13CO2. EDA, epidural group.

There were no significant changes in whole-body O₂ and CO₂ in both groups (Table 4). The respiratory quotient increased after surgery in the EDA group to higher values than in the control group (P < 0.05).

	Discussion

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Despite the well-established inhibitory effect of epidural local anesthetics on the hyperglycemic and endocrine response to surgery, glucose infusion in the present study caused an increase in plasma glucose levels more than 10 mmol/L, with or without epidural block. This finding gains clinical importance because acute hyperglycemia has been associated with impaired phagocytic capacity of polymorphonuclear leukocytes (7), dysfunction of the complement system (20), increased CO₂ production (5), stimulated sympathoadrenergic activity (6), and increased morbidity and mortality in patients after major surgery (8).

The measurement of plasma glucose concentration per se does not provide insight into the underlying metabolic changes, i.e., glucose production and uptake, and therefore, the kinetics of glucose metabolism were assessed in the present study by a stable isotope tracer technique. The suppressive effect of epidural block on glucose production is in agreement with findings showing a reduction of intraoperative splanchnic glucose release during combined glucose infusion and epidural block (12). However, it must be noted that splanchnic glucose release, as calculated from splanchnic blood flow and the arteriohepatic venous difference of glucose, is not an accurate measure of glucose production because it does not account for intestinal glucose uptake.

Despite the significant suppression of EGP by exogenous glucose in the EDA group, hyperglycemia occurred independently of the anesthetic technique used. This increase in plasma glucose concentration can therefore be largely ascribed to impaired glucose uptake, as reflected indirectly by reduced plasma glucose clearance. This finding is in agreement with two recent investigations demonstrating a decrease in plasma glucose clearance during major abdominal surgery in fasting patients with or without epidural block (11,19). Neuraxial block with epidural local anesthetic may completely abolish the endocrine stress response to lower abdominal (gynecological) surgery, as reflected in unchanged plasma concentrations of the counter-regulatory hormones cortisol, epinephrine, and norepinephrine (9). In contrast, this effect is less pronounced during major and upper abdominal procedures, which is most likely a result of the insufficient afferent somatic and sympathetic block (9). In accordance with this notion, the increase in plasma cortisol concentration observed in this study was attenuated but not completely blocked. Because cortisol represents an important mediator of the hyperglycemic response to surgery by counteracting the peripheral action of insulin on the glucose uptake system (21), it is suggested that the decrease in whole-body glucose uptake in the present study can be ascribed to the incomplete inhibition of the endocrine stress response to major abdominal surgery by epidural analgesia.

Gluconeogenesis contributes more than 90% to total glucose production under perioperative conditions, a consequence of the fasting-induced depletion of glycogen stores and the stimulatory effect of counter-regulatory hormones (22,23). Because muscle protein is broken down to supply amino acids serving as precursors for de novo glucose synthesis, it has been hypothesized that any suppression of gluconeogenesis may reduce protein breakdown (1). This assumption is supported by recent studies demonstrating a positive correlation between glucose production and protein breakdown in surgical patients (18,24). Thus, this the first study providing an integrated analysis of glucose and protein kinetics in patients receiving IV glucose during the acute phase of surgical trauma. Whole-body protein breakdown in the present protocol decreased to a similar extent in both groups, lending support to the assumption that protein catabolism is controlled by factors other than the demand for gluconeogenic precursors alone. Our finding of a depressed protein metabolism during surgery adds to our earlier results of a reduction in protein breakdown and oxidation by 20%, which occurred independently of the anesthetic technique used, i.e., inhaled, IV, or epidural (11,24,25). The fact that amino acid oxidation during glucose administration decreased by more than 50% and that protein synthesis was preserved indicates a protein-sparing effect of intraoperative hypocaloric glucose administration in both groups. However, it seems that the anticatabolic effect of glucose was most pronounced during the intraoperative period because amino acid oxidation increased two hours after the operation back to preoperative values.

It is of interest to note that in contrast to the present findings, epidural block facilitates the uptake and oxidative use of glucose infused at 4 mg · kg^-1 · min^-1 two days after abdominal surgery (18). This was accompanied by a decrease in amino acid oxidation, indicating a protein-sparing effect of epidural block in the presence of nutritional support. A possible explanation for the different anticatabolic properties of epidural block might be the more profound stress response with significantly greater circulating levels of counter-regulatory hormones during the intraoperative period compared with the postoperative phase.

In summary, the suppression of EGP by hypocaloric glucose infusion was more pronounced in patients receiving epidural block than in patients with general anesthesia alone. However, epidural analgesia did not enhance the anticatabolic effect of IV glucose during the acute phase of the stress response. Because significant hyperglycemia occurred independently of the type of anesthesia, it remains to be determined whether patients can benefit from intraoperative glucose administration.

	Acknowledgments

 
R.L. was awarded the CIHR (Canadian Institute of Health Research, Ottawa, Ontario, Canada) / AstraZeneca Ronald Melzack Pain Research Fellowship (Mississauga, Ontario, Canada). Generous financial support was also received from the Department of Anesthesiology, University Hospital of Ulm, Ulm, Germany.

We gratefully acknowledge Dr Judith Trudel for the permission to study her patients.

	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 (14) Citing Articles via Google Scholar Google Scholar Articles by Lattermann, R. Articles by Schricker, T. Search for Related Content PubMed PubMed Citation Articles by Lattermann, R. Articles by Schricker, T. Related Collections Surgery Monitoring (Non-cardiac) Regional Anesthesia