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Department of Anesthesiology, Rush Medical College, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, Illinois
Address correspondence to Christopher J. O’Connor, MD, Department of Anesthesiology, Rush Medical College, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL 60612. Address e-mail to coconnor{at}rush.edu
The application of epidural analgesia as an adjunct to general anesthesia continues to enjoy enthusiastic support among clinicians. Evidence of improved postoperative pulmonary function (1), favorable changes in bowel recovery after abdominal surgery (2,3), reduced hypercoagulability and graft thromboses after peripheral vascular surgery (4–6), and fewer thromboembolic complications after total joint arthroplasty (7), have reinforced the view that perioperative epidural neuraxial blockade not only provides superior analgesia (8), but also attenuates postoperative morbidity and mortality (9). The successful use of thoracic epidural analgesia/anesthesia (TEA) for the treatment of angina and ischemic heart disease (10–12) and the favorable results of improved analgesia when TEA is used after thoracotomy (1) have prompted investigations of TEA for cardiac surgery (13–15) with the expectation that cardiac sympathectomy and improved pulmonary function from enhanced analgesia will reduce the incidence of perioperative myocardial ischemia and infarction. Unfortunately, no studies of adequate size and statistical power have evaluated outcome when TEA is used during coronary artery bypass graft (CABG) surgery, nor has the fear of epidural hematoma formation and paraplegia subsided despite the absence of a single reported case of epidural hematoma after cardiac surgical procedures involving TEA (16). In this issue, Scott et al. (17) present the first randomized, prospective evaluation of the impact of perioperative TEA on outcome in a large series of patients undergoing CABG.
In their unblinded analysis of 400 patients with normal ventricular function undergoing CABG, Scott et al. (17) assessed the postoperative impact of TEA using 0.5% bupivacaine and clonidine administered via thoracic epidural catheters placed immediately before surgery. Their results indicate a reduction in the incidence of supraventricular arrhythmias (SVA), postoperative confusion, lower respiratory tract infections, and renal failure in TEA-treated patients compared with a control group treated with a target-controlled postoperative infusion of alfentanil. In addition, they also observed that TEA-treated patients were more often extubated within 4 h of arrival in the intensive care unit. Several aspects of their study, as well as the controversial issue of TEA for cardiac surgery, merit scrutiny.
The authors previously reported a similar effect of TEA on the incidence of SVA in a retrospective investigation of 218 patients undergoing CABG (18). Using a similar protocol in their current analysis of 418 patients, they chose the incidence of arrhythmias as the basis of their power analysis, estimating their study had a 90% power to detect a reduction in arrhythmias from 25% to 10%. The confirmation of fewer SVA with TEA is the most noteworthy and compelling (although not unexpected) finding of this report. Other investigators have reported lower catecholamine levels and slower heart rates after CABG in TEA-treated patients (14,19), a predictable consequence of cardiac sympathectomy. One confounding feature of Scott et al’s protocol is the inclusion of clonidine in the epidural infusion, since clonidine reduces sympathetic tone and heart rate (20,21). Although the epidural dose used (6–9 µg/h) is less than previously reported IV doses (70 µg/h) (20), the isolated impact of TEA with local anesthetic becomes less clear. In addition, postoperative ß-adrenoreceptor blockade significantly reduces the incidence of SVA after cardiac surgery (22), and it can be reasonably argued that perioperative administration of ß-adrenergic blocking drugs achieves the same outcome at less cost and with fewer serious risks than TEA.
The second notable finding of this study was the reduced incidence of lower respiratory tract infections, a result attributed to improved analgesia and enhanced ventilatory function; the latter outcome was supported by greater inspiratory lung volumes in a subset of patients in the TEA versus Control groups (985 mL vs 733 mL, respectively). Although the voluntary nature of these measurements and the lack of blinded evaluators weaken the causal link between TEA and improved ventilatory function, they represent a realistic mechanism to explain enhanced pulmonary function and reduced lower respiratory tract infections. Unfortunately, current data are inconclusive regarding the impact of TEA on postthoracotomy pulmonary function (23), and previous evidence suggests limited improvement in spirometric measurements when TEA is used for CABG (24); this is possibly related to the less severe pain typically encountered after median sternotomy compared with thoracotomy. Finally, the extended duration of analgesia in the current study in TEA-treated patients (96 h, compared with 72 h for patient-controlled analgesia-treated patients) may have altered the incidence of both SVA and respiratory events.
The investigators also established a decreased incidence of confusion in the TEA group, a not unexpected finding given the potential central nervous system effects of alfentanil. An unpredictable outcome, however, was the reduced incidence of renal dysfunction in the TEA group, suggested by the authors to be a possible consequence of clonidine’s influence on renal medullary function (25). This intriguing finding deserves further investigation, but can only be considered a preliminary observation because of the absence in this analysis of more specific data regarding established risk factors for renal dysfunction. A notable limitation of this study is the omission of Holter monitoring to assess the impact of TEA on postoperative myocardial ischemia, a predictable and potentially significant benefit of TEA. In this regard, the possible antithrombotic effect of TEA, coupled with cardiac sympathectomy and beneficial effects on the distribution of coronary blood flow (11), suggests a promising role for TEA in mitigating the incidence of perioperative myocardial infarctions. Indeed, Loick et al. (20) observed a decrease in postoperative troponin levels when TEA was used for CABG, suggesting an anti-ischemic effect of TEA. Unfortunately, the current study of Scott et al. (17) is underpowered to allow valid conclusions regarding the impact of TEA on perioperative myocardial infarction.
Countering the potential cardioprotective effect of TEA is the risk of hypotension secondary to bradycardia and reduced sympathetic tone. The authors provide limited documentation of the deleterious side effects of thoracic epidural blockade with 10 mL of 0.5% bupivacaine combined with clonidine. In contrast, several previous studies in CABG patients have shown larger intraoperative vasopressor requirements in TEA-treated individuals compared with controls (14,19), and the impact of hypotension on the incidence of myocardial ischemia in patients with critical coronary stenoses cannot be ignored. This aspect of the application of TEA during CABG requires further careful study in these at-risk patients.
If we accept the premise that TEA reduces pulmonary and cardiac morbidity after CABG, are the benefits offset by the potential risk of epidural hematoma formation from neuraxial anesthesia performed immediately before full heparin anticoagulation? It is unlikely that clinicians will widely adopt this approach for cardiac surgery until they are convinced that the risk of paraplegia from an epidural hematoma is infinitesimal and the clinical benefits well validated. A mathematical analysis and estimation of the risk of spinal cord injury from an epidural hematoma based on a large number of cases of TEA for cardiac surgery reviewed by Ho et al. (16), has been estimated with 95% confidence to be between 1:1,500 to 1: 150,000, a theoretical but not insignificant risk. However, most of these reports followed specific guidelines regarding TEA, such as inserting the epidural catheter the day before surgery, limiting the number of attempts at catheter placement, and delaying heparin administration for at least 60 min after catheter insertion (26,27). The current study is, therefore, not entirely analogous to previous reports, although the contemporary practice of same-day admission for CABG patients is a practical and economic barrier to catheter placement the day before surgery.
Additional considerations regarding the use of TEA for cardiac surgery include altered hemostasis after surgery and the appropriate timing of catheter removal, case cancellation because of "bloody taps," and delayed postoperative recognition of subtle neurologic deficits because of sedation, residual anesthetic effects, and continuing hemodynamic instability. In fact, spontaneous epidural hematomas and paraplegia in the absence of neuraxial anesthesia have been reported after cardiac surgery (28,29). Ultimately, one case of epidural hematoma and paraplegia will no doubt be unacceptable for most clinicians and despite the absence of a single report of paraplegia in this setting, many anesthesiologists will be reluctant to adopt this technique until significant and scientifically established improvements in outcome are fully validated. As previously questioned, just because nothing has gone wrong, is everything all right? (30) Given these considerations, TEA may be a potentially more attractive approach for off-pump or minimally invasive CABG, where anticoagulation is less intense and thoracotomy approaches more frequently used.
Although the report of Scott et al. (17) falls short of demonstrating a dramatic change in postoperative outcome after CABG, it represents a worthwhile and compelling effort that merits further study. The approach of these investigators to insert thoracic epidural catheters immediately before full anticoagulation will likely be the subject of some criticism, but they are to be commended for evaluating the impact of TEA in a meaningful and objective fashion, and for searching for answers in an area once considered forbidden territory.
References
This article has been cited by other articles:
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  M. A. Chaney Intrathecal and Epidural Anesthesia and Analgesia for Cardiac Surgery Anesth. Analg., January 1, 2006; 102(1): 45 - 64. [Abstract] [Full Text] [PDF]
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 G. H. Wheatley III, D. H. Rosenbaum, M. C. Paul, A. P. Dine, M. A. Wait, D. M. Meyer, M. E. Jessen, W. S. Ring, and J. M. DiMaio Improved pain management outcomes with continuous infusion of a local anesthetic after thoracotomy J. Thorac. Cardiovasc. Surg., August 1, 2005; 130(2): 464 - 468. [Abstract] [Full Text] [PDF]
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R. Dowling, K. Thielmeier, A. Ghaly, D. Barber, T. Boice, and A. Dine Improved pain control after cardiac surgery: results of a randomized, double-blind, clinical trial J. Thorac. Cardiovasc. Surg., November 1, 2003; 126(5): 1271 - 1278. [Abstract] [Full Text] [PDF]
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D. Amar and N. Scott Beta-Adrenergic Blocker Withdrawal Confounds the Benefits of Epidural Analgesia With Sympathectomy on Supraventricular Arrhythmias After Cardiac Surgery * Response Anesth. Analg., October 1, 2002; 95(4): 1119 - 1119. [Full Text] [PDF]
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B. J. Riedel and A. D. Shaw Thoracic Epidural Anesthesia & Analgesia in Patients Undergoing Coronary Artery Bypass Surgery Anesth. Analg., May 1, 2002; 94(5): 1365 - 1365. [Full Text] [PDF]
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