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*Department of Anesthesiology, Washington University, St. Louis, Missouri,
Department of Anesthesiology and General Intensive Care and
Anesthesiology and Intensive Care Medicine, Vienna General Hospital, University of Vienna, Austria;
Department of Anesthesiology, University of Berne, Switzerland; and
||Outcomes Research InstituteTM, University of Louisville, Kentucky
Address correspondence and reprint requests to Andrea Kurz, MD, Department of Anesthesiology, University of Berne, 3010 Berne, Switzerland. Address e-mail to kurza{at}msnotes.wustl.edu
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Abstract |
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IMPLICATIONS: Thoracic epidural anesthesia blunts the decrease of subcutaneous tissue oxygen tension caused by surgical stress and adrenergic vasoconstriction during major abdominal surgery. Consequently, combined general and epidural anesthesia helps to provide sufficient tissue oxygenation.
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Introduction |
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The first few hours after bacterial contamination constitute a decisive period during which infections are established (8). Perioperative management might thus be of major importance to reduce the incidence of surgical infections. For example, perioperative maintenance of normothermia and supplemental oxygen administration markedly decrease the incidence of wound infections (9,10). However, the effect of different anesthetic techniques on PsqO2 remains unknown. General anesthesia causes vasodilation both directly at the microvascular level (11,12) and by centrally inhibiting tonic thermoregulatory vasoconstriction (13). Neuraxial anesthesia also causes vasodilation by blocking sympathetic nerves (14). Predictably enough, epidural anesthesia, with or without general anesthesia, thus increases tissue oxygenation in the affected-blocked areas (15). Specifically, it has been shown that wound tissue oxygenation is more frequent in patients receiving postoperative pain treatment with epidural analgesia with local anesthetics in comparison with IV morphine analgesia (16). It remains unknown to what extent intraoperative systemic block of the surgical stress response caused by epidural anesthesia influences tissue oxygenation in unblocked areas during anesthesia and surgery. We thus tested the hypothesis that intraoperative subcutaneous oxygen partial pressure in the upper arm (an unblocked area) is greater when general and epidural anesthesia are combined than during general anesthesia alone.
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Methods |
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Patients were randomly and prospectively assigned with computer-generated randomization numbers to general anesthesia (n = 15) or general anesthesia with supplemental epidural anesthesia (n = 15) to the upper thoracic levels (T4). In both groups, patients received an epidural thoracic catheter for postoperative pain control at the level of T6-9 before the induction of general anesthesia. General anesthesia was induced with sodium thiopental (3–5 mg/kg) and 2.5 µg/kg of fentanyl. Vecuronium (0.1 mg/kg) was administered to facilitate tracheal intubation. Ventilation was mechanically controlled to maintain end-tidal carbon dioxide tension near 35 mm Hg.
Anesthesia was maintained with sevoflurane (0.7%–1.5%) in 30% oxygen/70% air. Supplemental oxygen was administered as required to maintain oxyhemoglobin saturation >95% in all patients. Sevoflurane administration was adjusted by the attending anesthesiologist, who was not involved in the study, with the goal of maintaining mean arterial blood pressure (MAP) within 20% of preinduction values. Supplemental bolus doses of IV fentanyl (0.1 mg) were delivered as required (increased heart rate [HR] or MAP more than 20% of baseline values).
In the combined anesthesia group, patients received a combination of general anesthesia and thoracic epidural anesthesia. After negative aspiration, a test dose of 3 mL of 2% lidocaine without epinephrine was injected. Subsequently, 6 to 10 mL of 0.5% ropivacaine was applied epidurally to establish a sensory block up to T4. Appropriate levels of epidural anesthesia were confirmed by the loss of sensation to pinprick before the induction of general anesthesia. During surgery, epidural block was maintained by continuous infusion of a 0.5% solution of ropivacaine via the epidural catheter at a rate of 0.05–0.1 mL · kg-1 · h-1. In the general anesthesia group, the epidural catheter was used in the postoperative period only.
After the induction of anesthesia, an 18-gauge arterial cannula was inserted into a radial artery. A central venous line was placed via the right internal jugular vein. In a subgroup of 20 patients (10 in each group), a pulmonary artery thermodilution catheter (93A-131–7F; Baxter Healthcare Corp, Irvine, CA) was inserted.
Before the induction of anesthesia, all patients received an initial dose of 10 mL/kg of lactated Ringer’s solution. Subsequently, we administered 10 mL · kg-1 · h-1 of lactated Ringer’s solution throughout surgery. Additionally, blood loss was replaced with crystalloid at a 4:1 ratio or colloid at a 2:1 ratio; supplemental fluid was given as required to maintain urine output exceeding 1 mL · kg-1 · h-1. Central venous pressure (CVP) was maintained near 10 mm Hg in all patients. Target minimum hematocrit, based on the patient’s age and cardiovascular status, was prospectively determined. Allogenic blood was administered only as required to maintain the prospectively determined target hematocrit.
MAP was kept within 20% of baseline measurements, which were obtained before the induction of epidural and general anesthesia. If MAP decreased, anesthetic management and fluid management were adjusted accordingly. No vasoactive drugs were administered. Patients were actively warmed with forced-air on the lower body to maintain intraoperative normothermia (Bair Hugger, Augustine Medical, Eden Prairie, MN) and IV fluid warming, whereas we strictly avoided local warming of the measurement site.
Demographic data, ASA status, preoperative laboratory values, and type and duration of surgery were recorded. All routine anesthetic, respiratory, and hemodynamic variables were also recorded. Detailed records of fluid management including urine output were kept. Inspired oxygen, end-tidal sevoflurane, and carbon dioxide concentrations were measured during anesthesia. Core temperature was measured in the distal esophagus (Mon-a-Therm®, Mallinckrodt Anesthesiology Products, St Louis, MO). Depth of anesthesia was continuously assessed via a Bispectral electroencephalogram monitoring system (Aspect Medical Systems, Inc, Newton, MA). All data were recorded in 15-min intervals during the whole study.
HR, MAP, and CVP were monitored continuously in all patients. In a subgroup of 10 patients in each group, we recorded mean pulmonary arterial pressure and pulmonary artery occlusion pressure. Cardiac output (CO) was measured hourly by thermodilution (mean value of three measurements, CO-Set; Baxter Healthcare Corp). Arterial and mixed venous blood gas analyses were performed hourly from simultaneously drawn samples. Cardiac index (CI), arterial-mixed venous oxygen content difference, oxygen delivery/consumption ratio (DO2/
O2 ratio), and oxygen extraction were calculated using standard formulae. Pressures were measured with reference to the midaxillary line.
Arterio-venous shunt flow in the left arm, which was exposed to room air, was evaluated with a forearm minus fingertip and skin-surface temperature gradient. Both were recorded with cutaneous Mon-a-Therm thermocouples. We considered skin-tempera-ture gradients 
0°C to indicate arteriovenous shunt vasoconstriction (17).
After the induction of anesthesia, silastic tonometers were inserted into the lateral left upper arm for measurement of PsqO2 and temperature. Each tonometer consisted of 15-cm tubing filled with hypoxic saline; 10 cm of the tubing was subcutaneously tunneled. A Clark-type oxygen sensor and thermistor (Licox, Gesellschaft für Medizinische Sondensysteme, GmBH, Kiel, Germany) were inserted into the subcutaneous part of the tonometer, as previously described (18).
In vitro accuracy of the optodes (in a water bath at 37°C) was ±3 mm Hg for the range from 0 to 100 mm Hg and ±5% for the range 100–360 mm Hg. Temperature sensitivity was 0.25% per degree celsius, thermistors were incorporated into the probes, and temperature compensation was included in the PsqO2 calculations. Optode calibration remained stable (within 8% of baseline value for room air) in vivo for at least 8 h. Optodes (oxygen sensors) were calibrated in room air (ambient pO2 = 154 mm Hg). For calibration purposes, a calibration card was inserted into the Licox device. The calibration data of the connected optode and other data were electronically stored on this card (factory calibration setting). All PsqO2 values measured before insertion were within 10% of 154 mm Hg. To exclude a significant drift of the optode (>10%), probes were again exposed to room air after each investigation. No significant drift was observed throughout the entire study.
After insertion of the tonometers, 30 min were allowed for electrode equilibration. Values were subsequently recorded at 15-min intervals throughout the entire duration of surgery.
Continuous data were compared using unpaired t-tests when the values were normally distributed. The Wilcoxon’s ranked sum test was used for continuous data that were not normally distributed. Nominal data were analyzed with either 
2 test or Fisher’s exact test depending on the sparseness of the data. Repeated measurements were documented at 15 min intervals; measurements with means of pulmonary arterial catheterization were performed hourly. Data were averaged over time during the whole study period (duration of surgery minus stabilization time of the oxygen sensors) within each patient and then averaged among the patients in each treatment group. Changes of tissue oxygenation over time were analyzed using repeated-measures analysis of variance and Scheffé F test. Data are expressed as mean ± SD or as number within each category; P < 0.05 was considered statistically significant.
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Results |
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The hemodynamic variables and oxygenation variables did not differ significantly between the groups during the study period (Tables 2 and 3). There were no significant differences in arterial oxygen or carbon dioxide tensions, pH value, or hemoglobin between the groups (Table 3).
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Discussion |
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Supplemental thoracic epidural anesthesia during major abdominal surgery potentially causes sympathectomy, thereby substantially influencing sympatho-adrenergic responses to surgical stress. Efferent sympathetic block caused by thoracic epidural anesthesia prevents a decrease in gastric intramucosal pH values (19) and increases intestinal blood flow (20).
In accordance with these studies, PsqO2 tension was significantly larger during combined anesthesia compared with general anesthesia (54.3 ± 7.3 mm Hg versus 42.1 ± 8.6 mm Hg). Specifically, PsqO2 decreased only slightly during combined anesthesia, whereas it showed a pronounced decrease during general anesthesia (Fig. 1). We assume that supplemental thoracic epidural anesthesia diminishes sympatho-adrenergic responses caused by surgical stimuli. Thus, it improves microcirculation and tissue oxygen partial pressure. The observed overall difference in PsqO2 between groups was approximately 12 mm Hg; after 225 intraoperative minutes, a maximum difference of 15 mm Hg was reached (Fig. 1). A similar difference (approximately 14 mm Hg) was observed in a recent study, which evaluated the effect of postoperative epidural analgesia on tissue oxygenation in the blocked area (16). It is likely that this effect was caused by the combination of block of the surgical stress response and the vasodilator property of the local anesthetics administered. Taken together with our results, this suggests that the observed increase in PsqO2 with epidural anesthesia is mainly caused by sympathetic block; the vasodilator effect of the local anesthetics per se might thus be minimal. This is consistent with a study by Treschan (15), which showed that epidural local anesthetics only slightly increase tissue oxygenation in healthy volunteers without surgical stress. However, all these studies were performed during different conditions and in different populations, and therefore, a final statement about the exact mechanisms cannot be made.
The most critical range of oxygen tension is between 0 and 40 mm Hg (7,21). PsqO2 values near 60 mm Hg are considered normal in euthermic, euvolemic, healthy volunteers breathing room air (22). However, under critical conditions, higher PsqO2 values are required by injured tissue to support adequate immune function. Whether our observed difference is able to decrease postoperative complications, such as infections or impaired wound healing, needs to be elucidated in further studies.
Continuous epidural ropivacaine administration had no significant influence on central hemodynamics during balanced general anesthesia and surgery. We found no beneficial effect of supplemental thoracic anesthesia on global oxygen transport. This suggests that our differences in PsqO2 were not caused by hemodynamic or global oxygen transport variances. CI and DO2/O2 are of only limited value when assessing peripheral tissue oxygenation. Also, peripheral perfusion and oxygenation can be impaired, whereas hemodynamics and clinical routine monitoring, such as urinary output, remain unchanged1 (23).
A limitation of our study is that we did not compare tissue oxygenation between both sites: the unblocked and blocked area. Tissue oxygenation was measured in the subcutaneous tissue of the upper arm only. We know that increasing tissue oxygenation in the intraoperative period is decisive in reducing surgical wound infections (10); thus, the value of our study lies in the information it provides on tissue oxygen tension during surgery. However, in clinical practice, surgical manipulation and a lack of access to the probes during surgery might cause instability of tissue oxygen values. Thus, intraoperative measurements adjacent to the surgical wound were impracticable in our study. However, the specific aim of our study was to evaluate systemic effects of neuraxial block on tissue oxygenation only. Consequently, our data do not provide information about possible local vasoactive effects of epidural administration of local anesthetics (15).
To obtain stable and comparable hemodynamics in the two groups, we adjusted general anesthesia according to the patients’ requirements. As to be expected, we used significantly less analgesic medication and inhaled anesthetic in the combined anesthesia group. These are drugs that might cause vasodilation themselves and thus might influence tissue perfusion and oxygenation. However, general anesthetics have only minor influence on the surgical stress response (24). In any case, if there were any effects on tissue oxygenation, the smaller dosage used in the combined anesthesia group would probably decrease tissue oxygenation, rather than increase it.
A further limitation might be that we had no possibility to evaluate the distribution of the sympathetic block during surgery. However, neither finger- nor skin-temperature gradients differed significantly between the groups, suggesting that changes in sympathetic outflow were restricted to thoracic segments during surgery. Thus, we can assume that our results represent systemic responses to sympathetic block only.
In summary, thoracic epidural anesthesia blunted the decrease of PsqO2 tension caused by surgical stress and adrenergic vasoconstriction during major abdominal surgery in the unblocked area. Consequently, supplemental thoracic epidural anesthesia might be beneficial to improve peripheral oxygenation during prolonged abdominal surgery.
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Acknowledgments |
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Mallinckrodt Anesthesiology Products, Inc. (St Louis, MO) donated the thermocouples we used. We appreciate the valuable assistance of Thomas Scheck, MD, and Angelika Nagele, RN.
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Footnotes |
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1 Hopf HW. Subcutaneous tissue oxygen tension in "well-resuscitated" trauma patients. Crit Care Med 1994;22:A60. 
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, combined anesthesia; •, general anesthesia.
