University Department of Anaesthesia and Pain Management, Leicester University and the Department of Obstetric Anaesthesia, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
Presented
in part at the Anaesthetic Research Society Meeting, St Georges
Hospital, London, November 1998 and at the Obstetric Anaesthetists
Association Annual Scientific Meeting, Liverpool, April,
1999.
Accepted for publication: March 30, 2000
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Abstract |
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Br J Anaesth 2000; 85: 46870
Keywords:anaesthetic techniques, epidural; analgesia, patient-controlled; anaesthetics, local, ropivacaine; anaesthetics, analgesics, opioid; anaesthesia, obstetrics
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Introduction |
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Methods and results |
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After i.v. access had been established and an infusion of crystalloid commenced, all patients had a combined spinalepidural (CSE) anaesthetic. The epidural space was identified at L23 or L34 using a loss of resistance to saline technique with the patient in a sitting position. Dural puncture was performed by a needle-through-needle technique with a Whitacre 26G needle; hyperbaric 0.5% bupivacaine 2.6 ml was injected into the intrathecal space. An epidural catheter was then inserted into the epidural space.
When surgery was complete, patients were randomized, by a sealed envelope technique, into one of two groups: group R (n=25) received PCEA 0.1% ropivacaine, bolus 5 mg, lockout 15 min, with 3 mg h1 background infusion. Group RF (n=25) received PCEA 0.1% ropivacaine/fentanyl 2 µg ml1, at identical settings to group R. The analgesic regimen was prepared by the anaesthetist managing the patient, who was not subsequently involved in data collection. It was commenced in the recovery room while the spinal block was still effective. Patients and nursing staff were blind to the group randomization.
Pain at rest and on movement (sitting forward) on a 100 mm VAS at 2, 4, 6, 8, 12 and 24 h, satisfaction with postoperative analgesia at 24 h (VAS) and the incidence of nausea and pruritus were recorded by the patients on a four-page individual patient diary. Dermatomal sensory level was noted using ethyl chloride spray at the commencement of the study and at 8 h. Motor block was evaluated using a modified Bromage scale by nursing staff who were familiar with these assessments. If patients had inadequate analgesia, supplementary rescue analgesia with oral codeine 30 mg/paracetamol 500 mg was available. Total PCEA consumption was noted.
Postoperative monitoring consisted of hourly respiratory rate, pulse rate and non-invasive blood pressure measurements for 4 h and thereafter at intervals of 4 h. Hypotension was defined as systolic blood pressure <90 mm Hg. Sedation was assessed on a four-point scale: 0=fully alert, 1=drowsy, eyes closed occasionally; 2=asleep but roused easily on speaking to the patient; 3=profoundly sedated, roused by physical stimulation.
Data
were analysed in GraphPad PrismTM, version 2.0. Physical
characteristics and satisfaction scores were compared using the unpaired
t-test. VAS pain and total analgesic consumption were
compared using the MannWhitney U-test. Contingency
tables were constructed for categorical data and analysed by
2 analysis with Yates correction. The prospective
study power calculation was based on analgesic data. Previous studies of
women after Caesarean section indicated a standard deviation of the order
of 30 mm in early postoperative pain scores. We took a VAS reduction
of 25 mm to be clinically significant, hence 24 patients were required
in each group to give an
value of 0.05 and a ß value of
0.2.
Although 25 patients were enrolled in each group, only 23 in group R and 24 in group RF were deemed eligible for statistical analysis. One patient was withdrawn from each group because of technical difficulties with the epidural catheter. Another patients data were lost from group R because of PCEA provider pump failure. A further two patients were withdrawn from the ropivacaine group at 12 h because of profound, prolonged motor block. They were included in the analysis as the only missing data were at 24 h.
The two groups did not differ in age, weight or parity. Patients receiving ropivacaine alone had significantly higher VAS pain scores at 6 and 8 h at rest and at 8 and 12 h on movement. Total analgesic consumption was less in the RF group than in group R and no patient in RF requested supplementary oral analgesia compared with eight patients in group R (P=0.005). There was no difference in the time to first request for supplementary analgesia. Patients in group RF had significantly higher scores for satisfaction with their postoperative analgesia compared with group R (P=0.045) (Table 1).
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Comment |
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We chose a background infusion of ropivacaine 0.1%, believing that it would provide an acceptable balance between adequate analgesia and minimal motor block. In retrospect however, it is clear that we failed in this objective because we underestimated the pain produced by Caesarean section in our patients. In a randomized, double-blind study of three solutions of ropivacaine/fentanyl for PCEA after lower abdominal surgery, 0.05% ropivacaine/fentanyl 1 µg ml1 produced equivalent analgesia to 0.2% ropivacaine/fentanyl 4 µg ml1. However, the latter group had a 30% incidence of motor block, compared with none in those receiving the lower concentration of ropivacaine.4 Our choice of ropivacaine 0.1% could reasonably have been expected not to aggravate motor weakness. Moreover, recent work has shown that the relative potency of ropivacaine compared with bupivacaine is only 0.6 and the EC50 for the minimum local anaesthetic concentration for ropivacaine in labour is approximately 0.16%.5 Hence, 0.1% ropivacaine should have been even less likely to produce motor block than 0.1% bupivacaine.
Although the difference is statistically significant only when patients with all grades of motor weakness are included, this unexpected finding is clinically important because even Bromage grade 1 weakness precludes ambulation. Inadvertent intrathecal spread of ropivacaine (via the small dural hole created by the spinal component of the CSE) could possibly explain our observations, although there was no suggestion of dural puncture in any of our patients. Indeed, it has been shown that dural puncture with a 26 gauge Whitacre spinal needle before epidural injection (as in the present study) increases the caudal, but not the cranial, spread of epidural local anaesthetics.6
It is also possible that low thoracic placement of the epidural catheter may have been more appropriate. Repeated introduction of boluses of local anaesthetic into the lumbar area may not provide analgesia in the lower thoracic dermatomes, yet accumulation may increase the risk of motor weakness in the lumbar dermatomes. Although there is also greater sensitivity of neural tissue to local anaesthetics during the later stages of pregnancy, this is an unlikely explanation because patients in group RF did not have as much leg weakness as those in group R. However, it is noteworthy that patients in group R received a significantly higher dose of ropivacaine than patients in group RF over the duration of the study, presumably because their analgesia was less satisfactory than in group RF.
An alternative explanation is an interaction between the two local anaesthetics. An experimental model of profound nerve block under spinal anaesthesia found that combinations of amide local anaesthetics could produce unpredictable prolongation of the block. Although the mechanism is unclear, these investigators postulated that local anaesthetics could interact at the sodium channel to prolong effective duration.7 Whether this effect could be more pronounced on motor as opposed to sensory nerves is unknown.
In conclusion, we found a higher incidence of motor weakness after 8 h in patients receiving PCEA ropivacaine compared with a ropivacaine/fentanyl mixture after bupivacaine spinal anaesthesia. The reason for this finding is unclear, but further studies are indicated to clarify the optimum dose regimen of epidural ropivacaine and fentanyl after spinal anaesthesia. In the interim, caution should be exercised when administering epidural ropivacaine after bupivacaine spinal anaesthesia.
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Footnotes |
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References |
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2 Muldoon T, Milligan K, Quinn P, et al. Comparison between extradural infusion of ropivacaine or bupivacaine for the prevention of postoperative pain after total knee arthroplasty. Br J Anaesth 1998; 80: 6801[ISI][Medline]
3 Owen MD, dAngelo R, Gerancher JC, et al. 0.125% ropivacaine is similar to 0.125% bupivacaine for labor analgesia using patient-controlled epidural infusion. Anesth Analg 1998; 86: 52731[Abstract]
4 Liu S, Moore J, Luo A, et al. Comparison of three solutions of ropivacaine/fentanyl for postoperative patient controlled analgesia. Anesthesiology 1999; 90: 72733[ISI][Medline]
5 Capogna G, Celleno D, Fusco P, et al. Relative potencies of bupivacaine and ropivacaine for analgesia in labour. Br J Anaesth 1999; 82: 3713
6 Suzuki N, Koganemaru M, Onizuka S, Takasaki M. Dural puncture with a 26-gauge spinal needle affects spread of epidural anesthesia. Anesth Analg 1996; 82: 10402[Abstract]
7 Hassan HG, Youssef H, Renck H. Duration of experimental nerve block by combinations of local anaesthetic agents. Acta Anaesthesiol Scand 1993; 37: 2857