Con: unreliable benefit after thoracotomy--epidural is a better choice.

C LINICAL CHOICES concerning thoracic analgesia should be informed by knowledge of the expected risks and benefits of a particular technique as well as how that technique compares in these respects with alternative choices. In the case of intrapleural anesthesia for thoracic analgesia after thoracotomy in particular, there is often inconsistent benefit of dubious merit, and the technique does not compare favorably with potential alternatives such as epidural analgesia. Intrapleural anesthesia was first reported by Relestad and Str0mskag in 1986.1 They described the techmque in 81 patients undergoing unilateral breast surgery, renal surgery, or cholecystectomy with a subcostal incision. Numerous reports followed attempting to define the technique's applicability, mechanism of action, and relative safety. The keys to understanding the limitations of intrapleural anesthesia lie m understanding the applied anatomy and physiology of the intrapleural space, as well as how drug administration affects, or fails to affect, elements of the nervous system. The intrapleural space exists as a potential space between the visceral and parietal pleurae. Laterally, the space is separated from the segmental intercostal nerves by the parietal pleura and the thin intercostalis intimus muscles. Medlally, in the paravertebral region, the space lies close to the proximal segmental intercostal nerves as well as to the epidural and subarachnoid spaces. Of note is that the posterior primary ramus of the segmental spinal nerve branches away before the spinal nerve gives rise to the segmental intercostal nerve. The paravertebral chain ganglia are also close to the intrapleural space. The distribution of drug solutions in the intrapleural space and their consequent effects are known to be influenced sigmficantly by the location of the catheter as well as the position of the chest after administration. InJected solutions seek the most dependent regions of the space for a given position and accumulate there. 2 The predominant mechanism of action for intrapleural anesthesia is accepted to be the diffusion of local anesthetic through the parietal pleura to reach the intercostal nerves, with production of multiple segmental intercostal nerve block. 3 Depending on access of local anesthetic to other neural elements, there also may be components of sympathetic nerve block, splanchnic nerve block, or even brachial plexus block. Experimental evidence 3 and clinical experience argue against epidural, subarachnoid, or other central nervous system mechanisms of action for mtrapleural anesthesia. Morphine via the intrapleural route does not appear to activate peripheral opioid receptors 4 or to have any effect greater than if administered systemically. 5 Pleural pathology, such as edema or inflammation, may limit access of the drug to neural elements and enhance systemic uptake, possibly leading to limited neural blockade 1 and systemic side effects such as seizures. 6 Open thoracostomy drainage tubes can remove as much as 30% to 40% of injected bupivacaine over a 4-hour period. 7 The most common potential indlcanon for thoracic analgesia is acute postthoracotomy pain. The goals of analgesic therapy in this setting are to provide patient comfort and maximize chest bellows function as well as overall homeostasis. Studies reporting on intrapleural anesthesia for this indication can be broadly categorized into two groups. The first group has sought to evaluate the general analgesic efficacy of lntrapleural anesthesia in this setting. In their 1994 review of postthoracotomy pain control techniques, Kavanagh et al s identified several randomized, prospective, double-blinded, and controlled studies of intrapleural bupwacaine for pain following thoracotomy. Symreng et al 9 compared intrapleural bupivacaine, 0.5%, with intrapleural saline at 8 and 16 hours after surgery. Patients receiving bupivacaine reported a significant but transient reduction in pain scores and opioid use lasting 2 to 5 hours after injection; however, there were no significant intergroup differences in total oploid consumption. Improvements in pulmonary function were shown in the bupivacaine patients only, but only lasted as long as the block. Mann et aF ° compared intrapleural bupivacaine, 0.25%, administered in 20-mL boluses every 4 hours for 48 to 72 hours after surgery compared with mtrapleural saline. There was reduced pain at 4, 24, and 72 hours in the bupwacame group. There were no differences in opioid consumption between the groups, and the difference in pain scores was not sigmficant at 48 hours. Schneider et al n compared intrapleural bupivacaine, 0.5%, with intrapleural saline in 30-mL doses every 4 hours for a total of 12 doses after surgery. They reported no differences in Visual Analog Scale (VAS) pain scores or analgesic requirements between the two groups. Elman et a112 reported on 40 mL of 0.25% or 20 mL of 0.5% intrapleural bupivacaine after thoracotomy and found that, although there were reductions in VAS pain scores, pain relief was not sufficient and was associated with high concentrations of plasma bupivacaine. Similarly, Ferrante et al reported on 0.5% bupivacainc administered via one or two intrapleural catheters 7 on the thoracotomy side. They concluded that there was a failure to achieve adequate intrapleural analgesia in postthoracotomy patients. In their report, Ferrante et al 7 illuminate the shortfalls of intrapleural anesthesia for postthoracotomy pare. They documented a 30% to 40% loss of bupivacaine over a 4-hour period via thoracostomy tube drainage. They also noted the consistent complaint of paravertebral pain associated with a lack of medial pinprick anesthesia on the thoracotomy side, suggesting a lack of anesthesia of the posterior ramus of the segmental spinal nerve. They con-