Anesth Analg 2002;94:1614-1616
© 2002 International Anesthesia Research Society
REGIONAL ANESTHESIA
Epidural Morphine Delays the Onset of Tourniquet Pain During Epidural Lidocaine Anesthesia
Chen-Hwan Cherng, MD DMSc*,
Chih-Shung Wong, MD PhD*,
Fang-Lin Chang, MD*,
Shung-Tai Ho, MD MS*, and
Chian-Her Lee, MD
Departments of *Anesthesiology and Orthopedics, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
Address correspondence and reprint requests to Chen-Hwan Cherng, MD, DMSc, 7F, No. 13, Lane 61, Wan-Shou Road, Mu-Ja, 116, Taipei, Taiwan. Address e-mail to cherng1018{at}sinamail.com
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Abstract
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We conducted a randomized, double-blinded study to examine the onset time of tourniquet pain during epidural lidocaine anesthesia either with or without morphine in the epidural solution. Forty-five patients undergoing knee surgery with a thigh tourniquet were randomly allocated into 3 groups of 15 patients each: epidural morphine (EM; epidural administration of 17 mL of 2% lidocaine plus 2 mg of morphine, followed by IV injection of 0.2 mL of normal saline), IV morphine (IVM; 17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by IVM 2 mg IV), and control (17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by 0.2 mL of normal saline IV). The onset time of tourniquet pain was recorded. The level of sensory block was determined by the pinprick method at the occurrence of tourniquet pain. Hemodynamic changes and side effects of EM were also recorded. The onset time of tourniquet pain from both the epidural injection and the tourniquet inflation were significantly longer in the EM group (103 ± 15 min and 80 ± 15 min, respectively) compared with the IVM group (74 ± 12 min and 50 ± 12 min, respectively; P < 0.05) and the Control group (67 ± 9 min and 45 ± 9 min, respectively; P < 0.05). The level of sensory block at the onset of tourniquet pain and hemodynamic changes were not different among the three groups. Only two and three patients in the EM group complained of nausea/vomiting and pruritus, respectively. Respiratory depression was not observed in any patient. We conclude that epidural injection of the mixture of 2 mg of morphine and 2% lidocaine solution delayed the onset of tourniquet pain during epidural lidocaine anesthesia without significant morphine-related side effects.
IMPLICATIONS: We examined the effect of epidural morphine on the onset of tourniquet pain during epidural lidocaine anesthesia. We found that the addition of 2 mg of morphine to epidural 2% lidocaine significantly delayed the onset of tourniquet pain without increasing morphine-related side effects.
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Introduction
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Pneumatic tourniquets are often used in limb surgery to decrease blood loss and provide a clear surgical field. Tourniquet-induced pain may occur during spinal or epidural anesthesia despite adequate sensory block (1–4). Its occurrence is more frequently observed during epidural anesthesia than spinal anesthesia (1,5). Tourniquet-related pain is described as a poorly localized, dull, tight, aching sensation at the site of tourniquet application. The mechanism of tourniquet pain is poorly understood. It has been proposed that it is mediated by unmyelinated, slow-conducting C fibers (6–8). Epidural morphine (EM) may inhibit the C fiber-related afferent nociceptive impulses through spinal mechanisms (9). The purpose of this study was to examine the effect of EM on tourniquet pain during knee surgery under epidural lidocaine anesthesia.
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Methods
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This was a randomized, double-blinded, prospective study. After approval by the human research review committee of our institute, informed consent from each patient was obtained. Forty-five patients, ASA physical status I–II, scheduled for knee surgery with a thigh tourniquet, in whom the anticipated inflation time was more than 60 min, were included. The patients were randomly allocated into three groups—EM, IV morphine (IVM), and control (C)—with 15 patients in each group. Routine monitoring included electrocardiogram, arterial blood pressure, heart rate, and pulse oximetry during surgery. With patients in the left lateral decubitus position, catheters were inserted at the L3-4 interspace and advanced 5 cm into the epidural space. A test dose of 2% lidocaine 3 mL (Astra, Sodertalje, Sweden) containing 1:200,000 epinephrine (freshly added) was administered to eliminate intrathecal or IV injection. Three minutes later, the patients in Group EM received epidural administration of 17 mL of 2% lidocaine (containing 1:200,000 epinephrine) plus 2 mg (0.2 mL) of morphine, followed by IV injection of 0.2 mL of normal saline. The patients in Group IVM received epidural administration of 17 mL of 2% lidocaine (containing 1:200,000 epinephrine) plus 0.2 mL of normal saline, followed by IV injection of 2 mg (0.2 mL) of morphine. The patients in Group C received epidural administration of 17 mL of 2% lidocaine (containing 1:200,000 epinephrine) plus 0.2 mL of normal saline along with an IV injection of 0.2 mL of normal saline. The speed of epidural lidocaine administration was consistent in all groups, at approximately 3 mL/10s.
Midazolam IV in 1- to 2-mg increments was given for intraoperative sedation. During the surgical preparation, the operated limb was lifted until the tourniquet was inflated to 350 mm Hg. When patients complained of pain during surgery, it was recorded as tourniquet pain if the pain was not related to the surgical field and was described as a dull, tight, aching sensation at the area of the tourniquet application. At the onset of tourniquet pain, the time was recorded, and the level of sensory block was determined by pinprick method with a 21-gauge needle in a cephalad to caudal fashion along the left anterior axillary line by a blinded observer. Once tourniquet pain occurred, an additional 8 mL of 2% lidocaine (containing 1:200,000 epinephrine) was administered epidurally and was repeated every 40 min thereafter until the end of surgery. Arterial blood pressure and heart rate were measured every 5 min after epidural injection. Hypotension (systolic blood pressure <100 mm Hg or a decrease of >30% from baseline) was treated with 5 mg of IV ephedrine as needed. Side effects of EM, such as nausea, vomiting, pruritus, or respiratory depression, were recorded during surgery.
The results are expressed as mean ± SD or median (range) for the level of sensory block. The differences in onset time were analyzed with analysis of variance and the Student-Newman-Keuls test for post hoc comparison. The levels of sensory block were compared by using the Kruskal-Wallis test and the Dunn’s multiple comparison procedure for post hoc comparison. The incidences of side effects among groups were analyzed by Fisher’s exact test. A P value <0.05 was considered statistically significant.
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Results
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The three groups were similar with respect to age, sex, weight, and height. The anesthetic characteristics of the three groups are shown in Table 1. There was no difference in the duration of tourniquet inflation among the three groups. Both the onset times of tourniquet pain calculated from the time of epidural injection and from the time of tourniquet inflation were significantly longer in the EM group than in the IVM and C groups. The level of sensory block at the onset of tourniquet pain and the changes in arterial blood pressure and heart rate were not different among the three groups. Two and three patients in the EM group complained of nausea/vomiting and pruritus, respectively. The incidence of side effects did not reach statistical significance. Respiratory depression was not observed in any patient.
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Discussion
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Tourniquet pain may occur during spinal or epidural anesthesia despite adequate sensory block (3,10). The pathway associated with tourniquet pain remains unclear. It was proposed to be mediated by C fibers (6–8). Differential sensitivity of nerve fibers to lidocaine was demonstrated by Gissen et al. (11), who showed that the C and A-ß fibers were more resistant to lidocaine-induced conduction block than A-
fibers. It is believed that the A- fibers are responsible for pinprick, or sharp pain, which is often used for testing sensory blockade during spinal or epidural anesthesia. Therefore, the C fiber-mediated tourniquet pain may occur when A- fibers are still blocked. From the results of Gissen et al. (11), the concentrations of lidocaine to block C and A-ß fibers were similar. Rocco et al. (12) demonstrated that during spinal anesthesia, there was no correlation between the level of sensory block to pinprick and the occurrence of tourniquet pain, but the level of sensory block to light touch, mediated by A-ß fibers, appeared relevant to the onset of tourniquet pain. Therefore, the level of sensory block to touch may be used as an indicator for the occurrence of tourniquet pain.
The results of this study showed that the addition of 2 mg of morphine to a 2% lidocaine solution significantly delayed the onset of tourniquet pain during epidural anesthesia. The mechanisms by which morphine delays the onset of tourniquet pain are not clear. Kaneko et al. (13) demonstrated that epidural coadministration of morphine and lidocaine produced synergistic and prolonged analgesic effects on both somatic and visceral nociception in rats. Lidocaine and morphine exert their independent actions via separate and distinct mechanisms. Lidocaine blocks impulses by inhibiting sodium channels, whereas morphine acts via the opioid receptors to produce an inhibitory effect on the intracellular second messengers. In fact, lidocaine not only blocks the sodium channels, but also affects the synaptic transmission. Kirota et al.1 reported that lidocaine dose-dependently inhibited the cyclic adenosine monophosphate formation in Chinese hamster ovary cells. Moreover, Li et al. (14) demonstrated that lidocaine inhibited both substance P binding and substance P-evoked increases in intracellular calcium. Morphine exerts an inhibitory effect on neuronal transmission via both pre- and postsynaptic mechanisms (15). In addition, opioids can also open potassium channels and result in membrane hyperpolarization and decreased neuronal excitability (16). Therefore, epidural coadministration of morphine and lidocaine may synergistically inhibit neuronal excitability. In this study, although the onset of tourniquet pain was delayed in the EM group, the sensory block levels to pinprick at the onset of tourniquet pain were not different among the three groups (T10 or T11). This suggests that EM may potentiate the sensory block during epidural lidocaine anesthesia.
EM produces a spinal effect via opioid receptors in the dorsal horn of the spinal cord (9). EM may also exert a supraspinal action by distribution from systemic absorption and by intrathecal cephalad spread. In this study, IVM had no effect on the onset time of the tourniquet pain during epidural lidocaine anesthesia. This suggests that, in this study, morphine acted primarily at the spinal level.
EM-related side effects were observed in only two patients with nausea/vomiting and three patients with pruritus. No respiratory depression was observed in any patient. This infrequent incidence of the side effects might be due to the moderate dose of EM (2 mg) we used.
In conclusion, the addition of 2 mg of morphine to 2% lidocaine (containing 1:200,000 epinephrine) delayed the onset of tourniquet pain during epidural anesthesia without significant morphine-related side effects.
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Footnotes
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1 Kirota K, Appadu BL, Grandy DK, et al. Effect of lidocaine on cAMP formation with recombinant opioid receptors expressed in Chinese hamster ovary cells [abstract]. Anesthesiology 1998;89: A801. 
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Accepted for publication January 16, 2002.
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Abstract
Introduction
