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Skip Navigation LinksHome > December 2000 - Volume 91 - Issue 6 > Intrathecal Anesthesia: Ropivacaine Versus Bupivacaine
Anesthesia & Analgesia:
doi: 10.1097/00000539-200012000-00030
Regional Anesthesia and Pain Medicine

Intrathecal Anesthesia: Ropivacaine Versus Bupivacaine

Malinovsky, Jean-Marc MD, PhD*; Charles, Florence MD*; Kick, Ottmar MD*; Lepage, Jean-Yves MD*; Malinge, Myriam MD, PhD*; Cozian, Antoine MD*; Bouchot, Olivier MD†; Pinaud, Michel MD†

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*Service d’Anesthésie-Réanimation Chirurgicale, and †Service d’Urologie, Hôtel-Dieu, Nantes Cedex, France

August 1, 2000.

Address correspondence and reprints requests to J-M Malinovsky, MD, Department of Anesthesiology, Hôtel-Dieu, 44093 Nantes Cedex 1, France. Address e-mail to jmmalino@chu-nantes.fr.

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Abstract

We compared intrathecal ropivacaine to bupivacaine in patients scheduled for transurethral resection of bladder or prostate. Doses of ropivacaine and bupivacaine were chosen according to a 3:2 ratio found to be equipotent in orthopedic surgery. One hundred patients were randomly assigned to blindly receive either 10 mg of isobaric bupivacaine (0.2%, n = 50) or 15 mg of isobaric ropivacaine (0.3%, n = 50) over 30 s through a 27-gauge Quincke needle at the L2-3 level in the sitting position. Onset and offset times for sensory and motor blockades and mean arterial blood pressure were recorded. Pain at surgical site requiring supplemental analgesics was recorded. Cephalad spread of sensory blocks was higher with bupivacaine (median level, cold T4 and pinprick T7) than with ropivacaine (cold T6 and pinprick T9) (P <0.001). Eight patients in Group Ropivacaine received IV alfentanil (P <0.01). Onset time (mean ± sd) to T10 anesthesia and offset time at L2 were not different (bupivacaine = 13 ± 8 min, 127 ± 41 min; ropivacaine = 11 ± 7 min, 105 ± 29 min). Complete motor blockade occurred in 43 patients with bupivacaine and in 41 patients with ropivacaine (not significant). Total duration of motor blockade was not different. No difference in hemodynamic effects was detected between groups. No patient reported back pain. We conclude that 15 mg of intrathecal ropivacaine provided similar motor and hemodynamic effects but less potent anesthesia than 10 mg of bupivacaine for endoscopic urological surgery.

Implications: Inadequate intrathecal anesthesia was observed in 16% of patients with 15 mg of ropivacaine, whereas intensity and duration of motor blockade was not different in comparison to 10 mg of bupivacaine. Ropivacaine appears to be less potent than bupivacaine at doses used in spinal anesthesia.

Epidural ropivacaine is used extensively for labor, caesarean delivery, and postoperative analgesia. It appears to be less potent and induces less intense motor blockade than bupivacaine (1). This may be because ropivacaine is an l-isomer, whereas bupivacaine is a racemic mixture. Ropivacaine also seems less toxic to the cardiovascular (2) and central nervous systems (3).

Spinal anesthesia by using single-shot intrathecal lidocaine is associated with transient neurological symptoms (4), regardless of the concentration of the injected solution (5). Moreover, cauda equina syndromes were described after repeated injections of higher concentrated solutions (5%) through small-diameter catheters (6), underscoring the neurotoxic potential of intrathecal lidocaine. Other local anesthetics have been examined for intrathecal use as an alternative to intrathecal lidocaine. Among them, small doses of ropivacaine were compared with bupivacaine. In the range of 2–4 mg, intrathecal ropivacaine induces the same analgesic effects with weak motor blockades as 2.5 mg of bupivacaine (7). Larger doses (4–12 mg) used in volunteers appear to be half as potent (8). Doses from 8 to 12 mg were administered for outpatient knee arthroscopies (9); the dose-ratio ropivacaine:bupivacaine showing similar profiles of effects was 3:2, and, at equal doses, anesthesia was less intense using ropivacaine (9).

As the comparison between ropivacaine and bupivacaine was described only in volunteers and only for knee arthroscopy, we designed a comparative study in patients scheduled for urological surgery using spinal anesthesia.

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Methods

After Research and Ethics Committee approval and informed consent were obtained, 100 patients scheduled for endoscopic resection of the bladder or prostate, or urethral surgery using spinal anesthesia were included in this randomized, double-blinded study.

Premedication consisted of 10 mg of oral midazolam and prophylactic antibiotics. Patients received no intravascular volume loading before spinal anesthesia. They were monitored by electrocardiogram and an automatic blood-pressure cuff. Intrathecal injections were performed in the operating room by using a 27-gauge Quincke needle (Becton-Dickinson, Le Pont de Claix, France) at the L2-3 level with the patient in sitting position. The distal port of the needle was also oriented cranially. Patients were randomly assigned to two groups, receiving either 10 mg of bupivacaine (density 1.006, pH 6.5, 285 mOsm/L) (Group B, n = 50) or 15 mg of ropivacaine (density 1.006, pH 5.56, 291 mOsm/L) (Group R, n = 50).

We choose isobaric solutions because only dextrose-free ropivacaine solutions are available. Anesthetic solutions were prepared in the operative room by a physician not involved in the spinal injection. The commercial solutions were diluted with 0.9% saline as needed, and the volume of each anesthetic solution was 5 mL. The dose of bupivacaine was chosen as being clinically effective for such surgical procedures (10). Although the equipotent ratio between bupivacaine and ropivacaine was 2:1 in volunteers (4 mg of hyperbaric bupivacaine was equivalent to 8 mg of hyperbaric ropivacaine injected in the lateral position) (8), we choose to inject ropivacaine and bupivacaine in a dose-ratio of 3:2, as previously determined in surgical patients (9). Intrathecal injections were performed over a 30-s period in all groups. Patients were placed in lithotomy position with no elevation of the torso after the injection. Patients were then tested every 3 min up to the maximal spread of blockade, and then every 10 min until recovery of anesthesia.

Sensory blockade was assessed by using pinprick and cold (iced tube) on each side of the midthoracic line, and patients were asked about sensation at the site of surgery. The quality of intraoperative anesthesia was scored by the patients every 10 min during surgery. A score of 0 corresponded to no sensation at the site of surgery, a score of 1 to sensation at the site of surgery but no pain, and a score of 2 to painful sensation at the site of surgery with the request by the patient of supplemental analgesics (bolus of 0.5 mg of IV alfentanil). The degree of motor blockade was scored at the level of the thigh by using a four-point scale: a score of 0 was recorded when no motor effects occurred; a score of 1 corresponded to a decrease in muscle strength with the ability to flex the thigh; a score of 2 to the inability to flex the thigh despite muscle contractions; and 3 to the complete paralysis of thigh flexion. Onset time for blockade was defined as the time between injection and maximal blockade. Block duration was defined as the period between injection and recovery from blockade.

Mean arterial blood pressure was recorded every 3 min throughout the study and surgery. Patients were considered hypotensive when mean arterial blood pressure decreased >25% from the baseline value; they received boluses of IV ephedrine (3 mg) every 3 min before vascular loading with crystalloid solution. A decrease in heart rate <40 bpm was treated with 0.1 mg/kg of IV atropine.

Each day during the first four postoperative days and 1 mo later, patients were asked by a physician, who had not participated in anesthesia, about back pain radiating into the legs and buttocks.

Data were presented as mean ± sd or median as appropriate. Comparisons between groups for onset time of sensory and motor blockades and cephalad spread of sensory blocks were performed by using a Mann-Whitney U-test. The ability to obtain a complete motor blockade and the requirement of supplemental analgesics and of vasoconstrictors were compared by using a contingency table. Mean arterial blood pressure changes were compared by using analysis of variance for repeated measures. The significance level was set at P < 0.05.

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Results

Demographic data were not different between groups. Mean ± sd age, weight, and height of patients were 68 ± 4 yr, 71 ± 8 kg, and 171 ± 7 cm in the ropivacaine group, and 68 ± 7 yr, 71 ± 8 kg and 170 ± 6 cm in the bupivacaine group. Surgical procedures were performed with a similar level of skill between groups. No patient reported back pain during 4 wk of follow-up.

Cephalad spread of sensory blocks was higher with bupivacaine (median level, pinprick T7 and cold T4) than with ropivacaine (pinprick T9 and cold T6, P < 0.001), as can be seen in Figure 1. Onset time to anesthesia at level T10 was not different between groups (Table 1).

Figure 1
Figure 1
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Table 1
Table 1
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Nineteen patients complained of sensation at surgical site, 2 with bupivacaine and 17 with ropivacaine. However, the sensations at site of surgery were painful in only 8 patients, all in the group receiving ropivacaine (P = 0.003). These patients with inadequate anesthesia received a median dose of 1.5 mg of IV alfentanil (range 0.5–2.5 mg). Offset time for pinprick anesthesia at level L2 was longer with bupivacaine than with ropivacaine, but was not different for cold (Table 1). The profiles of anesthetic duration are reported in Figure 2 and were not different between ropivacaine and bupivacaine.

Figure 2
Figure 2
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Complete motor blockade occurred in 43 patients receiving bupivacaine and in 41 receiving ropivacaine (not significant). No difference was found in the intensity of motor blockade at each measurement interval when using both local anesthetics (Figure 3). Onset time and total duration of motor blockades were not different between groups (Table 1).

Figure 3
Figure 3
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The number of patients with hypotension was 22 in bupivacaine and 19 in ropivacaine groups, and mean ± sd doses of ephedrine were 8 ± 10 mg with bupivacaine and 6 ± 9 mg with ropivacaine (not significant).

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Discussion

Our main result is that 15 mg of ropivacaine is less potent than 10 mg of bupivacaine for intrathecal anesthesia. In the present study, 16% of the patients receiving ropivacaine for endoscopic surgery had inadequate spinal anesthesia. This agrees with previous reports. The dose of 15 mg of intrathecal ropivacaine was associated with 20% inadequate anesthesia in abdominal surgery (11) and with 5% in lower limb surgery (12). The equipotent ratio between ropivacaine and bupivacaine would be closer to the findings of McDonald et al. (8), who found ropivacaine half as potent in volunteers. Gautier et al. (9) found that 8 mg of bupivacaine was equipotent to 12 mg of ropivacaine; however, the level of anesthesia required for knee surgery is lower than for endoscopic urological surgery, which requires at least a T10 level of anesthesia. This may explain the difference observed between our series and the study done by Gautier et al. (9). However, as we tested only a single dose of each local anesthetic, it is difficult to draw any firm conclusion.

We found that the cephalad extent of anesthesia was significantly lower with ropivacaine. Wahedi et al. (11) found that mean cephalad extent of anesthesia was related to dose, T10 with 15 mg and T8 with 22.5 mg of ropivacaine. Interestingly, isobaric solutions were injected with the patients in the sitting position as in the present study. In contrast, McDonald et al. (8) reported a higher cephalad extent of anesthesia for ropivacaine, which may be related to hyperbaric solutions injected in the lateral position. We found a lower cephalad extent of anesthesia associated with less intense anesthetic blockade in the ropivacaine group, resulting in the requirement of supplemental analgesics to perform surgery.

It may be argued that the volume of diluted anesthetic solutions may alter the cephalad extent of anesthesia. However, there are large interindividual variations in the total volume of cerebrospinal fluid (13), and dilution does not significantly affect the spread of intrathecal anesthesia (10). Finally, the major determinant for the spread of intrathecal anesthesia is the dose of local anesthetic injected (14).

One of the reasons to use intrathecal ropivacaine and to replace lidocaine, especially for ambulatory spinal anesthesia, is that, at equal doses, it has a shorter duration of action than bupivacaine. Moreover, the main theoretical advantage of intrathecal ropivacaine would be to induce less motor blockade than bupivacaine, as shown after the epidural administration (1). Unfortunately, we found that motor blockade between groups was of the same intensity and duration. This may be related to the dose of ropivacaine used, whereas smaller doses up to 4 mg did not induce motor blockade (7).

Neurotoxic effects have been associated with intrathecal lidocaine, prompting the research of alternatives to lidocaine, especially for ambulatory anesthesia. The use of intrathecal ropivacaine was suggested because it does not affect the spinal cord blood flow (15) and does not induce neurotoxic effects after intrathecal administration in dogs (16) and rabbits (17). Clinical studies are not numerous, and irritative signs have not been reported in 200 patients with different doses of ropivacaine: 30 patients received 2 to 4 mg (7), 120 received 8 to 12 mg (9), and 50 received 15 mg of ropivacaine in our series.

In contrast to 10 mg of bupivacaine, 15 mg of ropivacaine was ineffective for endoscopic procedures of the lower urologic tract. Though ropivacaine seems less potent, the intensity and duration of motor blockade were similar. These results in surgical patients are in agreement with studies comparing ropivacaine to bupivacaine at smaller doses in volunteers (8) and for orthopedic surgery (9).

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References

1. Zaric D, Nydahl PA, Philipson L, et al. The effects of continuous epidural infusion of ropivacaine (0.1%, 0.2% and 0.3%) and 0.25% bupivacaine on sensory and motor blockade in volunteers: a double-blind study. Reg Anesth 1996; 21: 14–25.

2. Reis S, Haggmark S, Johansson G, Nath S. Cardiotoxicity of ropivacaine-a new local anaesthetic agent. Acta Anaesthesiol Scand 1989; 33: 93–8.

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6. Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72: 275–81.

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9. Gautier PE, de Kock M, van Steenberge A, et al. Intrathecal ropivacaine for ambulatory surgery. Anesthesiology 1999; 91: 1239–45.

10. Malinovsky JM, Renaud G, Le Corre P, et al. Intrathecal bupivacaine in humans: effects of volume and baricity on spinal effects. Anesthesiology 1999; 91: 1260–6.

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13. Hogan Q, Prost R, Kulier A, et al. Magnetic resonance imaging of cerebrospinal fluid volume and the influence of body habitus and abdominal pressure. Anesthesiology 1996; 84: 1341–9.

14. Greene NM. Distribution of local anesthetic solution within the subarachnoid space. Anesth Analg 1985; 64: 715–30.

15. Kristensen JD, Karlsten R, Gorth T. Spinal cord blood flow after intrathecal injection of ropivacaine and bupivacaine with or without epinephrine in rats. Acta Anaesthesiol Scand 1998; 42: 685–90.

16. Ganen EM, Vianna PTG, Marques MEA, et al. Effects of large volume of 2% lidocaine and 1% ropivacaine on dogs spinal cord [abstract]. Anesthesiology 1998; 89: A1415.

17. Malinovsky JM, Charles F, Benhamou D, et al. Intrathecal ropivacaine in rabbits : pharmacodynamic and local neurotoxic effects [abstract]. Anesthesiology 1999; 91: A884.

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