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*Department of Anesthesia and Perioperative Care and Outcomes ResearchTM Group, University of California-San Francisco, San Francisco, California; and Departments of
Anesthesiology and Intensive Care Medicine and
Urology, Donauspital, Vienna, Austria
Address correspondence to Robert Greif, MD, Department of Anesthesia and Perioperative Care, University of California-San Francisco, 374 Parnassus Ave., 3rd Floor, San Francisco, CA 94143-0648. Address e-mail to greif{at}compuserve.com
| Abstract |
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Implications: We conclude that pleural analgesia significantly prolongs the time until postoperative opioid was first requested and halves the total required dose. These data indicate that pleural analgesia is effective and provides a significant opioid-sparing effect.
| Introduction |
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Despite the large positive experience with pleural analgesia after cholecystectomy (12,13), only a few studies have evaluated the method for treatment of nephrectomy pain (1416). Furthermore, the results have been mixed (3,17). Variable efficacy reported in the literature (14,15,17) contrasts with our excellent clinical experience with the technique.
Baude et al. (15) compared epidural opioids with pleural bupivacaine and with IV opioids. Pleural analgesia was found to be ineffective, with visual analog scale (VAS) scores >5. Murphy (14) reported inadequate analgesia in four of eight patients after nephrectomy. He "felt that the posterior extension of the operation scar might have contributed to inadequacy of the block" and that inserted drainage tubes may also have contributed.
We therefore tested the efficacy of 20 ml of pleural bupivacaine 0.25%, administered at 6-h intervals the first 48 h after nephrectomy. No drainage tubes were placed. Efficacy was defined by a VAS score and the extent to which pleural analgesia reduced the need for IV opioids.
There is no consensus about the terminology used to designate pleural analgesia (3,18,19). When the method was first used, it was described as "interpleural" analgesia. However, "parietal and visceral pleura are continuous around the hilar structures and the right and left pleura sacs are distinct. Therefore, an injection of a local anesthetic through a needle that has penetrated the parietal membrane, but not the visceral membrane, is intrapleural analgesia" (18). The accumulation of fluid within the pleural space is also called pleura effusion. The epidural space is also a potential space. We do not use "interepidural analgesia" or an "intradural catheter." As Baumgarten (19) suggested, the best solution to this controversy would be to abandon the two prefixes and to call the technique "pleural block" or "pleural analgesia."
| Methods |
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The patients were premedicated with ranitidine and oxazepam the evening before and 7 AM on the day of surgery. Anesthesia was induced with propofol (1.52.5 mg/kg) and fentanyl. Endotracheal intubation was facilitated by the administration of vecuronium. Anesthesia was maintained with isoflurane in a nitrous oxide/oxygen mixture. Before emergence from anesthesia, the neuromuscular blockade was antagonized by the IV administration of atropine and neostigmine.
At the end of surgery, patients were randomly assigned to two treatment groups based on computer-generated codes: 1) pleural analgesia combined with the IV administration of the opioid piritramid and 2) IV piritramid alone. In patients assigned to pleural analgesia, an pleural catheter was positioned at the sixth intercostal space in the midaxillary line with the patient in the supine position just before anesthesia was discontinued during spontaneous ventilation.
The pleural catheter was inserted, as previously described (20), via a 16-gauge Tuohy needle connected to a Y-piece. Briefly, one arm of the Y-piece was connected to a balloon, which collapsed when the needle was introduced into the negative intrathoracic pressure of the pleural cavity. The catheter (0.6 x 1.0 mm diameter; Pleurocert®; Fa. B. Braun Melsungen, Melsungen, Germany) was then inserted through the other arm of the Y-piece to a distance of 5 cm. This closed system minimizes the likelihood of pneumothorax. The first 20-mL bolus of bupivacaine 0.25% was given immediately after catheter insertion. Patients were subsequently given 20 mL of pleural bupivacaine 0.25% every 6 h until the second postoperative day. The catheter was removed approximately 48 h after insertion.
In both groups, pain was treated with IV piritramid, a pure µ receptor agonist. One milligram of the synthetic opioid piritramid is equipotent to 0.8 mg of morphine hydrochloride (21). Every 6 h, pain was recorded by using the VAS, and patients were asked whether they needed pain relief medication. Opioids were given in the range of 7.515 mg at any time by the nurses on patient demand, but not more often than at 6-h intervals.
A preoperative chest radiograph was obtained per clinical routine; 1 h after pleural puncture, a chest radiograph was obtained for detection of a possible pneumothorax. Pain was evaluated at 6-h intervals with a 10-cm VAS (0 = no pain and 10 = excruciating pain). The times until pain medication was first requested and total opioid requirement during the first 2 postoperative days were recorded.
Potentially confounding variables and total opioid dose were evaluated by using two-tailed, unpaired t-tests. The times until pain medication was first requested in each group were compared by using a Mann-Whitney U-test. Pain scores over time were compared by using a one-way analysis of variance. Data are presented as means ± SD. P < 0.05 was considered statistically significant.
| Results |
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Patient characteristics were comparable in the two study groups (Table 1), as was the duration of surgery (2.8 ± 1.0 h in the pleural catheter group versus 2.9 ± 0.6 h in the IV opioid group) and intraoperative fentanyl use (0.6 ± 0.3 vs 0.6 ± 0.2 mg). VAS scores for pain were relatively low and were comparable in each group (Fig. 1).
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| Discussion |
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The mechanism of action of local anesthetics injected between the parietal and visceral pleura is understood as retrograde diffusion to reach the intercostal nerves, the splanchnic nerves, and the sympathetic chain, which are adjacent to the parietal pleura. Using computed tomography, Stromskag et al. (23) found gravity-dependent intercostal nerve blockade. With patients in the supine position, these authors found analgesia from T5 to L1, and the paravertebral area was covered by local anesthetic solution. In the paravertebral area, the sympathetic chain and the splanchnic nerves are separated from the pleura cavity only by the parietal pleura. Similar results were described by van Kleef et al. (22). Five and a half dermatomes were blocked for approximately 8 h using bupivacaine 0.25% pleurally after cholecystectomy.
Pain scores of patients given pleural analgesia supplemented with piritramid were similar to those of patients given piritramid alone. Furthermore, the scores were relatively low in each case. Thus, our major finding is that pleural analgesia significantly prolonged the time until postoperative opioid was first requested and decreased the total required dose by a factor of 2. These data indicate that pleural analgesia is effective and provides a substantial opioid-sparing effect.
As previously reported, sufficient postoperative analgesia improves lung function by facilitating early patient mobilization. Early mobilization also reduces atelectasis in basal and dorsal lung compartments. However, opioid administration is associated with postoperative hypoventilation. As might be expected, pleural analgesia improves pulmonary function and postoperative oxygenation compared with IV opioids (13,24).
Pleural analgesia is associated with a number of potential complications, most notably pneumothorax and local anesthetic toxicity (2,3,25). IV opioids are similarly associated with risks, especially ventilatory depression and cognitive impairment that may restrict early postoperative ambulation. We did not observe any substantial complications in either group. However, too few patients were included in our protocol to evaluate the relatively uncommon adverse effects associated with either method.
Plasma concentrations of bupivacaine during pleural analgesia have been evaluated in numerous previous studies (5,12,22). The estimated threshold plasma concentration associated with the onset of central nervous system toxicity for bupivacaine is thought to be 24 µg/mL (3). We chose 20 mL of pleural bupivacaine 0.25% every six hours because this dose is unlikely to be associated with toxic plasma concentrations (3). van Kleef et al. (22) also found no difference between the use of 0.5% and 0.25% bupivacaine after cholecystectomy. They found a slightly lower VAS score for pain (approximately 2) but a higher opioid requirement in both groups (29 mg in the first 24 hours) than we found in the local anesthetic group.
In contrast to previous reports (14,15), we showed in our investigation that using a timed regimen of pleural local anesthetic is effective after nephrectomy. Frenette et al. (24) reported a improvement of lung function using pleural analgesia, and an additional reduction in stress response and catecholamine release, resulting in an early normalization of postoperative bowel function, was found by Kastrissios et al. (13).
The risk of pneumothorax is reduced when the recommended technique of insertion of the catheter is used (2). Although high plasma local anesthetic concentrations are attained with pleural analgesia, clinical toxicity is rarely reported (3,25). Little correlation was found between plasma bupivacaine concentration and central nervous system toxicity. The rate of change in plasma concentration seems to be more important in determining clinical toxicity than the absolute plasma bupivacaine concentration (3,25).
In summary, 20 mL of pleural bupivacaine 0.25% every six hours provided a substantial opioid-sparing effect during recovery from nephrectomy and extended the time until opioids were needed for pain relief. This indicates that the technique is effective and reduces the need for postoperative opioids with their associated potential complications
| Acknowledgments |
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We gratefully acknowledge the support and generous assistance of Daniel I. Sessler, MD, Department of Anesthesia and Perioperative Care, University of California-San Francisco.
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