| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
,¶,#
,||,¶
*Department of Anesthesia and General Intensive Care, Vienna General Hospital,
Ludwig Boltzmann Institute, and
Department of Anesthesia and Intensive Care Medicine, University of Vienna, Vienna, Austria;
Departments of Anesthesia and
||Anesthesiology, Washington University, St. Louis, Missouri; and
¶Outcomes ResearchTM Institute and
#Department of Anesthesiology, University of Louisville, Louisville, Kentucky
Address correspondence and reprint requests to Dr. Andrea Kurz, 660 So. Euclid Ave., St. Louis, MO 63110. Address e-mail to kurza{at}msnotes.wustl.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
IMPLICATIONS: Epidural anesthesia significantly increased subcutaneous tissue oxygenation in the thigh both with and without general anesthesia. Although each increase was statistically significant, previous work suggests that the magnitude of these changes is unlikely to markedly reduce the risk of surgical wound infection.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
At a given arterial oxygen partial pressure, perfusion is the primary determinate of subcutaneous oxygenation (5). The effect of different anesthetic techniques on subcutaneous perfusion and tissue oxygen tension has not been well established. Most general anesthetics are direct peripheral vasodilators (6–8). They also indirectly cause vasodilation by inhibiting tonic thermoregulatory vasoconstriction (9), thereby increasing arteriovenous shunt perfusion 10-fold (10). It is thus likely that general anesthesia increases peripheral tissue oxygen tension. Neuraxial anesthesia usually causes a sympathectomy, thereby substantially increasing perfusion in blocked regions (11,12). Neuraxial anesthesia is thus also likely to increase tissue oxygenation. However, the effect size of this increase on tissue oxygenation is not known. We therefore tested the hypothesis that epidural anesthesia increases tissue oxygenation in the legs with and without anesthesia.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Each volunteer participated on two randomly assigned study days: 1) general anesthesia, and 2) epidural anesthesia followed by combined epidural and general anesthesia. The studies started at similar times on each day, and the volunteers fasted during the preceding 8 h. Volunteers rested supine on a standard operating room table set in chaise lounge position on top of a water mattress heated to 37°C. Ambient temperature was maintained near 22°C.
A catheter was inserted in a right antecubital vein for fluid and drug administration. Because even subtle hypovolemia reduces tissue oxygenation (13), volunteers were given 15 mL/kg Ringer’s lactate solution IV upon arrival in the laboratory. They were subsequently given 2 mL · kg-1 · h-1 Ringer’s lactate solution for the remainder of the study; an additional 15 mL/kg was infused just before the induction of general anesthesia on both study days. Intravenous fluids were warmed during the entire study period. The volunteers breathed 30% oxygen from a sealed face mask connected to a valved anesthesia machine during the control period and during epidural anesthesia.
On one study day, anesthesia was induced with 1.5 mg/kg propofol and 6% sevoflurane in 30% oxygen. A pharyngeal airway was inserted after loss of the eyelash reflex. Subsequently, anesthesia was maintained with sevoflurane—1.5% end-tidal concentration in 30% oxygen. Spontaneous ventilation was assisted as necessary to maintain end-tidal carbon dioxide tension near 40 mm Hg. After 1.5 h, anesthesia was discontinued.
On the other study day, a catheter was inserted into the epidural space through an 18-gauge Tuohy needle. A test dose of 3 mL of mepivacaine, 1.5% with epinephrine 1:100.000, was given. At the appropriate time, 1.5% mepivacaine without epinephrine was titrated to produce a sensory block near T8. The sensory block was subsequently evaluated at 10-min intervals by loss of cutaneous cold sensation and loss of response to pinprick. A continuous 0.75% plain mepivacaine infusion was adjusted as necessary to maintain the designated level. A skin-temperature gradient (14) <0°C was considered evidence of arteriovenous shunt dilation (15).
After 1.5 h of epidural anesthesia, general anesthesia was induced and maintained as described above. The epidural infusion of mepivacaine was maintained throughout combined anesthesia. After 2 h of general anesthesia, sevoflurane was discontinued; the sensory block level was evaluated, and the mepivacaine infusion was discontinued.
Morphometric and demographic characteristics, and all routine anesthetic, respiratory, and hemodynamic variables were recorded. Core temperature was measured with a thermocouple positioned adjacent to the left tympanic membrane.
Arteriovenous shunt flow in the left arm was evaluated with a forearm minus fingertip, skin-surface temperature gradient; shunt flow in the left leg was similarly evaluated with a calf minus toe gradient (14). Both were recorded with cutaneous Mon-a-Therm thermocouples. We considered skin-temperature gradients 
0°C to indicate arteriovenous shunt vasoconstriction (16).
Silastic tonometers were inserted into the lateral left upper arm and lateral left thigh for measurement of subcutaneous tissue oxygenation and temperature. New tubes were inserted each study day after the skin was numbed with 1 mL of lidocaine (1%). Each tonometer consisted of a 15-cm tube filled with hypoxic saline, of which 10 cm was tunneled subcutaneously. 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 (17).
In vitro accuracy of the optodes (in a water bath at 37°C) is ±3 mm Hg for the range 0–100 mm Hg and ±5% for the range 100–360 mm Hg. Temperature sensitivity is 0.25%/°C, but thermistors are incorporated into the probes and temperature compensation is included in the subcutaneous oxygen tension (PsqO2) calculations. Optode calibration remains stable (within 8% of baseline value for room air) in vivo for at least 8 h. At least 30 min were allowed for electrode equilibration. Values were subsequently recorded at 10-min intervals for 30 min.
Within each volunteer, we averaged the following values: 1) the final 30 min of unanesthetized baseline, 2) the final hour of epidural anesthesia, 3) the final hour of general anesthesia, and 4) the final hour of combined epidural and general anesthesia. Our primary outcomes were the effect of epidural anesthesia on subcutaneous leg and arm tissue oxygenation with and without general anesthesia. We thus first compared unanesthetized baseline values with those obtained during epidural anesthesia. We then compared values during general anesthesia alone with values obtained during the combination of general and epidural anesthesia. In both cases, comparisons were based on paired, two-tailed t-tests; P < 0.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Potential confounding factors were similar with and without epidural anesthesia, including blood pressure, heart rate, oxygen saturation, and core temperature. Tissue oxygenation in the arm and thigh were virtually identical at baseline, and arm oxygenation remained unchanged during epidural anesthesia. However, thigh subcutaneous oxygen partial pressure increased by 9 ± 2 mm Hg, from 54 ± 8 to 63 ± 7 mm Hg (P < 0.001, Table 1).
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
General anesthesia also influences peripheral perfusion. First, general anesthetics reduce the threshold for thermoregulatory vasoconstriction by 2°–4°C, depending on the anesthetic type and dose. It is important to recognize though that arteriovenous shunts are restricted to acral skin, mostly on the fingers and toes. Second, general anesthetics directly dilate peripheral vessels (22). During general anesthesia, arteriovenous shunts were dilated in both the arms and legs and remained unchanged during the combination of epidural and general anesthesia. Nonetheless, the combination of general and epidural anesthesia increased subcutaneous oxygen partial pressure by 8 ± 3 mm Hg in the thighs without altering oxygen tension in the arms.
Although epidural anesthesia significantly increased thigh tissue oxygenation with and without general anesthesia, the magnitude of the increase was relatively small (i.e., 8 and 9 mm Hg). Inadequately treated surgical pain, for example, decreases tissue oxygenation approximately 25 mm Hg (19). Smoking—which is clearly associated with infection risk (23)—reduces PsqO2 by a similar fraction (20). Hopf et al. (3) observed that the risk of surgical wound infections was inversely related to tissue oxygen tension. However, increases from 55 to 65 mm Hg reduced the infection risk only approximately 5%. Similarly, supplemental oxygen, which increases subcutaneous partial pressure by approximately 50 mm Hg, halves infection risk (4). Extrapolating these findings to our current results, we suggest that a 10-mm Hg increase in tissue oxygenation will reduce the risk of infection by only approximately 10%. Available data thus suggest that increases in tissue oxygenation near 9 mm Hg are unlikely to substantially reduce infection risk and do not, per se, justify use of epidural anesthesia.
We evaluated unstimulated volunteers rather than surgical patients because it allowed us to carefully control the study circumstances and accurately measure both arm and thigh tissue oxygenation. A limitation of this approach, however, is that our volunteers were unstimulated, whereas surgery inevitably provokes a sympathetic response. The extent to which surgical stimulation and resulting sympathetic activation alters cutaneous perfusion and oxygenation remains unknown, but may be substantial. During surgical stress, the combined effect of vasodilation plus the suppression of the surgical stress response by sympathetic blockade might have a clinically important effect on tissue oxygenation. A recent article by Buggy et al. (24) showed an increase in subcutaneous tissue oxygenation of approximately 14 mm Hg in postsurgical patients under epidural anesthesia. This suggests that the effect size in stimulated patients after surgery is larger than in our unstimulated volunteers.
In unanesthetized humans, differences of only a few tenths of a degree centigrade are sufficient to provoke thermoregulatory vasoconstriction (25). But during general anesthesia, the interthreshold range (temperatures not triggering thermoregulatory defenses) increases 10- to 20-fold to 2°–4°C (10). The vasoconstriction threshold is further reduced when epidural and general anesthesia are combined (26). In our actively warmed volunteers, core temperature was slightly but significantly greater during combined epidural and general anesthesia than during epidural anesthesia alone. However, the difference was only 0.4°C, which is far too small to trigger thermoregulatory vasoconstriction during general anesthesia. Consequently, skin-temperature gradients were similar with and without epidural anesthesia, and it is highly unlikely that core temperature altered tissue oxygenation.
Thigh tissue temperatures increased approximately 1°C during epidural anesthesia. However, our optodes are temperature-corrected; tissue oxygen partial pressures thus remain accurate over a wide range of tissue temperatures. As might be expected, mean arterial blood pressure was slightly lower during combined epidural and general anesthesia than during general anesthesia alone. However, the difference was only 5 mm Hg, which is unlikely to have much altered PsqO2.
In summary, epidural anesthesia increased thigh subcutaneous tissue oxygenation approximately 9 mm Hg without anesthesia. A similar 8-mm Hg increase was observed when epidural anesthesia was added to general anesthesia. Although each increase was statistically significant under the specific conditions of this study (i.e., unstimulated volunteers), previous work suggests that the magnitude of the increases is unlikely to markedly reduce the risk of surgical wound infection and does not, per se, justify the use of epidural anesthesia for that purpose.
|
Acknowledgments |
|---|
Mallinckrodt Anesthesiology Products, Inc. (St. Louis, MO) donated the thermocouples we used. We appreciate the valuable assistance of Ozan Akça, MD, Thomas Scheck, MD, and Natascha Sommer, BS.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. H. Bakri, H. Nagem, D. I. Sessler, R. Mahboobi, J. Dalton, O. Akca, E. E. Roselli, and S. R. Insler Transdermal Oxygen Does Not Improve Sternal Wound Oxygenation in Patients Recovering from Cardiac Surgery Anesth. Analg., June 1, 2008; 106(6): 1619 - 1626. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
