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Anesth Analg 2005;100:921-928 © 2005 International Anesthesia Research Society doi: 10.1213/01.ANE.0000146437.88485.47
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Abstract |
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High thoracic epidural anesthesia/analgesia (HTEA) for coronary artery bypass grafting (CABG) surgery may have myocardial protective effects. In this prospective randomized controlled study, we investigated the effect of HTEA for elective CABG surgery on the release of troponin I, time to tracheal extubation, and analgesia. One-hundred-twenty patients were randomized to a general anesthesia (GA) group or a GA plus HTEA group. The GA group received fentanyl (7–15 µg/kg) and a morphine infusion. The HTEA group received fentanyl (5–7 µg/kg) and an epidural infusion of ropivacaine 0.2% and fentanyl 2 µg/mL until postoperative Day 3. There were no differences in troponin I levels between study groups. The time to tracheal extubation [median (interquartile range)] in the HTEA group was 15 min (10–320 min), compared with 430 min (284–590 min) in the GA group (P < 0.0001). Analgesia was improved in the HTEA group compared with the GA group. Mean arterial blood pressure poststernotomy and systemic vascular resistance in the intensive care unit were lower in the HTEA group. We conclude that HTEA for CABG surgery had no effect on troponin release but improved postoperative analgesia and was associated with a reduced time to extubation.
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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High thoracic epidural anesthesia/analgesia (HTEA) for coronary artery bypass graft (CABG) surgery promotes effective analgesia and sympatholysis and attenuates the stress response to surgery (1,2). In experimental conditions, HTEA reduces myocardial infarct size (3), possibly by improving myocardial oxygen balance. HTEA provides effective pain relief for patients with unstable angina and myocardial infarction; it reduces the major determinants of myocardial oxygen demand while maintaining coronary artery perfusion pressure (4,5). Balancing these potential benefits of HTEA is concern regarding epidural hematoma and permanent spinal cord damage with neuraxial block in patients who are fully heparinized for surgery.
Most randomized controlled studies in this area have focused on hemodynamic effects and the stress response to surgery. Studies assessing the important issue of potential cardioprotective effects of HTEA have yielded conflicting results. The release of cardiac troponin I (cTnI) has been shown to be a sensitive and specific marker of myocardial cell necrosis, with significant prognostic importance after cardiac surgery (6,7). Priestley et al. (8) found no difference in troponin levels between general anesthesia (GA) alone and GA plus HTEA groups, yet Loick et al. (9) found significantly reduced troponin T levels in their HTEA group. The aim of this prospective randomized study was to investigate the effect of HTEA for elective CABG surgery on postoperative release of biochemical markers and electrocardiograph (ECG) changes of myocardial ischemia/infarction. Although the time to tracheal extubation has been reduced by the use of HTEA in many studies, it can be influenced by multiple factors and varies greatly among institutions (10). Therefore, a secondary aim of this study was to assess the effect of HTEA on time to tracheal extubation in our institution. In addition, although HTEA has been shown in a number of studies to improve postoperative analgesia (1,8,11), analgesic regimens and their efficacy are also institution specific, and thus a third aim of our study was to assess the effect of HTEA on the quality of postoperative analgesia.
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Methods |
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The St. Vincent's Hospital human research ethics committee approved this prospective randomized controlled trial, and written informed consent was obtained from all patients. All patients scheduled for elective CABG surgery (using cardiopulmonary bypass (CPB)) were eligible. Exclusion criteria were emergency or repeat CABG surgery, combined valve and CABG surgery, aspirin ingestion within 6 days of surgery, a platelet count <150 x 109/L, an international normalized ratio >1.1, active neurological disease, and cutaneous disorders at the epidural insertion site. Patients were randomized the day before surgery to the GA group or the combined GA and HTEA group. The random-allocation sequence was computer-generated in permuted blocks of four and enclosed in sequentially numbered opaque sealed envelopes.
Patients randomized to the HTEA group had an epidural catheter (20-gauge; Portex, Hythe, Kent, UK) inserted the day before surgery at T1-2 or T2-3 by using a midline approach and loss-of-resistance-to-saline technique. Epidural catheters were inserted with patients sitting, by using an 18-gauge needle with the bevel directed cephalad, advanced into the epidural space 4 cm, and flushed with saline. Patients received their usual cardiac medications on the day of surgery. Premedication consisted of temazepam 20 mg and ranitidine 150 mg orally and morphine 0.10–0.15 mg/kg IM 2 h before anesthetic induction.
After initiation of ECG monitoring (leads II and V5 monitored) and insertion of invasive monitoring (radial artery cannula and pulmonary artery catheter), epidural block was established with 5 mL of ropivacaine 1% and fentanyl 50 µg. The block was assessed 20 min later by using loss of temperature sensation to ice, with success defined as a block over the T1 to T6 dermatomes. If required, the block was extended with 2 mL of ropivacaine 1%.
GA was induced with midazolam (0.05–0.1 mg/kg), fentanyl (7–15 µg/kg for the GA group and 5–7 µg/kg for the HTEA group), propofol (20-mg increments as required), and rocuronium (0.6 mg/kg). GA was maintained with propofol 3–6 mg · kg–1 · h–1. Further doses of rocuronium 10 mg were given only for overt patient movement, with no additional rocuronium given after CPB. Intraoperative hemodynamic management was standardized although, to represent routine practice, anesthesiologists defined acceptable limits to optimize individual patient management. Hypotension was treated with volume, metaraminol, or ephedrine; hypertension was treated with propofol 0.25–1 mg/kg, additional fentanyl, a volatile drug, or glyceryl trinitrate; tachycardia was treated with propofol 0.25–1 mg/kg or a ß-adrenoceptor blocker; and bradycardia was treated with ephedrine. All patients received heparin (300 IU/kg and 10,000 IU in the pump prime) and 
-aminocaproic acid (5 g before CPB and 5 g in the pump prime). Further heparin (100 IU/kg) was administered to maintain an activated clotting time more than 450 s at all times during CPB. CPB was performed with a noncoated circuit, membrane oxygenator, and nonpulsatile flow via a roller pump at 2.0–2.4 L · min–1 · m–2. Myocardial protection consisted of an initial dose of antegrade and retrograde blood cardioplegia (composition: potassium 20 mmol, aspartate 14 mmol, glutamate 14 mmol, magnesium 5 mmol, bicarbonate 15 mmol, and lidocaine 100 mg). Maintenance of arrest was achieved with intermittent retrograde blood cardioplegia (composition: potassium 8–12 mmol, aspartate 7 mmol, and bicarbonate 10 mmol) at the completion of each anastomosis. Cardioplegia was delivered at 25°C–30°C, with no crystalloid added. Phenylephrine 0.25–0.5 mg or isoflurane was used to maintain mean arterial blood pressure (MAP) between 65 and 90 mm Hg. Patients were separated from CPB after completion of grafting and rewarming to at least 36.5°C. Heparin was reversed with protamine 3 mg/kg. Further protamine (0.5–1 mg/kg) was given to return the activated clotting time to baseline or as initial management of bleeding.
Samples of blood for cTnI and creatine kinase myocardial fraction (CK-MB%) were collected preinduction and 12 and 24 h after aortic cross-clamp release, consistent with published recommendations (7,12–15). cTnI was measured by using the Abbott AxSYM analyzer (Abbott Laboratories, North Chicago, IL; reference value for cTnI, <0.6 µg/L; upper limit of measurement, 50 µg/L). The reference value for CK-MB% was <8. Twelve-lead ECGs were recorded before surgery and on postoperative Days 1 and 5 and were assessed by 2 observers blinded to group allocation and postoperative clinical course. Observers were specifically asked to note new persistent Q waves >0.04 s and new ST segment depression or elevation (>0.1 mV at 0.08 s after the J point) in at least 2 contiguous leads of the same vascular territory. Transmural infarction was defined as new Q waves and cTnI >15 µg/L at 24 h1 (13).
Hemodynamic measurements were recorded immediately before induction, 5 min after tracheal intubation, 1–2 min poststernotomy, and 10 min after separation from CPB. Measurements consisted of heart rate, MAP, mean pulmonary arterial pressure, central venous pressure, pulmonary artery occlusion pressure (PAOP), cardiac index (mean of three determinations by thermodilution), and systemic vascular resistance (SVR). Baseline left ventricular (LV) function was scored after induction by using transesophageal echocardiography based on a 16-segment model (16). Segments were scored as 1, normal; 2, mild hypokinesis; 3, severe hypokinesis; 4, akinesis; 5, dyskinesis; and 6, aneurysmal. An LV score was calculated by totaling the scores of the 16 segments. After CPB, the LV was assessed for new segmental wall motion abnormalities (SWMAs). Intraoperative and postoperative vasoactive drug requirements were recorded.
To facilitate early tracheal extubation, the propofol infusion was ceased at sternal closure, and minute ventilation was reduced to stimulate spontaneous ventilation. The time to tracheal extubation was measured from the time of surgical dressings. The anesthesiologist tracheally extubated patients in the operating room if extubation criteria—respiratory rate 10–20 breaths/min, responsiveness to voice, end-tidal CO2 <50 mm Hg, Sao2 >94% with a fraction of inspired oxygen of 1.0, hemodynamic stability, minimal chest drain output (not requiring transfusion or consideration for surgical reexploration) and temperature >35.9°C—were achieved within 30 min. For patients not extubated in the operating room, postoperative management of ventilation and extubation followed existing unit guidelines (17). Patients were required to respond appropriately to voice, have an acceptable ventilatory pattern and arterial blood gas analysis, and be hemodynamically stable. The first postextubation arterial blood gas (at approximately 30 min), complications, chest tube drainage, and day of discharge were recorded. Hemodynamic measurements were repeated in the intensive care unit (ICU) at two or more time points.
The GA group received an initial loading dose of morphine 0.1–0.2 mg/kg after separation from CPB and infiltration of ropivacaine 3 mg/kg into chest drain sites. Pain management in the ICU followed existing guidelines (17), including titration of morphine increments (1 mg) and commencement of a morphine infusion (after tracheal extubation) that continued until the morning of postoperative Day 2. In the HTEA group, an epidural infusion (ropivacaine 0.2% and fentanyl 2 µg/mL) was commenced 1 h after the induction of GA at an hourly rate equal to the required initial loading volume and was continued until the morning of postoperative day 3. If epidural analgesia was inadequate, the infusion was increased by 2 mL/h after a bolus of 2 mL. All patients received acetaminophen 1 g rectally at the completion of surgery. Pain rescue medication for both groups consisted of indomethacin 100 mg/12 h and oxycodone 5 mg/6 h. HTEA patients with a failed block received a morphine infusion as was used in the GA group.
Pain scores were measured with a visual analog scale (VAS) of 0–100 mm at 4 time points (separated by 4–6 h) during the first 24 h after tracheal extubation and at 2 time points (separated by 8–12 h) in the second and third 24-h periods after surgery. VAS pain scores were measured at rest and with coughing. Side effects and complications of analgesia were recorded at each analgesia assessment. Sedation was graded as 0, fully alert; 1, mildly drowsy; 2, moderately drowsy, easily rousable; 3, very drowsy but rousable; and 4, difficult to rouse or unrousable. Nausea was graded as 0, no nausea; 1, nausea but no vomiting; and 2, nausea and vomiting. Motor and sensory block were recorded in the HTEA group. Motor block in the upper limb was graded as 0, none; 1, mild hand weakness; 2, elbow weakness; and 3, weakness involving the shoulder. A research nurse or investigator usually performed these assessments. After hours, some of the assessments were performed by appropriately briefed ICU nurses and anesthesiology residents.
A formal sample size determination based on cTnI was not possible because cTnI data after CABG surgery with the Abbott AxSYM analyzer were not available at the time of study inception. The confidence interval for differences in median cTnI levels between groups was calculated to assess the precision of our data and, hence, the adequacy of our sample size. Nonparametric confidence intervals were calculated using Confidence Interval Analysis® software (BMJ Books, London, UK).
For our secondary end-point, sample size was calculated by using a mean time to tracheal extubation of 240 min, with an sd of 200 min (17). A clinically significant difference was determined to be a 50% reduction; this required a sample size of 45 in each group. Between-group analyses were performed with the Mann-Whitney U-test or Student's t-test, depending on the distribution and character of the data. Bonferroni's correction was used for multiple comparisons for hemodynamic data. Categorical data were compared by using Fisher's exact test. Time to tracheal extubation was analyzed with Kaplan-Meier survival curves and log-rank tests for differences between groups. The level of significance was taken as 0.05. Data were analyzed with StatView 4® (Abacus Concepts, Berkeley, CA) and Stata® Version 7.0 (Stata Corporation, College Station, TX).
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Results |
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One-hundred-twenty patients were randomized to 2 groups of 60 from December 1999 to March 2002. All patients were included in the analysis. Patient and surgical characteristics are listed in Table 1. There was a more frequent prevalence of cerebrovascular and peripheral vascular disease in the HTEA group (Table 1). Epidural blockade was successful in 58 of 60 patients. The two patients with nonfunctional epidural catheters were analyzed as being in the epidural group (i.e., intention to treat) but received analgesia with a morphine infusion as if in the GA group. All patients had baseline cTnI levels <0.3 µg/L.
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Epidural blockade required a median initial loading dose of 7 mL of ropivacaine, resulting in median upper and lower levels of sensory block of C5 (range, C3 to T1) and T10 (range, T3 to L3), respectively. The HTEA group had a significantly reduced MAP (78 vs 94 mm Hg) and SVR (994 vs 1261 dynes · s · cm–5) preinduction and had reduced MAP poststernotomy (83 vs 97 mm Hg) compared with the GA group. There were no other significant intraoperative hemodynamic differences between groups, nor were requirements for metaraminol and ephedrine different (Table 2). The fentanyl dosage (based on protocol) was significantly smaller in the HTEA group [median (interquartile range; IQR), 5.2 µg/kg (4.4–6.1 µg/kg)] than in the GA group [12.0 µg/kg (10.1–13.8 µg/kg)]. The intraoperative midazolam dosage was significantly smaller in the HTEA group [0.044 mg/kg (0.026–0.058 mg/kg)] than in the GA group [0.056 mg/kg (0.035–0.068 mg/kg)]. The intraoperative propofol dosage was not significantly different between groups: HTEA group, 16.3 mg/kg (13.4–18.4 mg/kg); GA group, 17.3 mg/kg (14.6–21.5 mg/kg). The GA group received morphine 0.12 mg/kg (0.1–0.12 mg/kg) after CPB. There were 21 patients with new SWMAs. Fifteen SWMAs had resolved by the completion of surgery. The distribution of SWMAs (persistent and resolving) was not different between groups.
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Time to tracheal extubation was significantly less in the HTEA group [15 min (10–320 min)] than in the GA group [430 min (284–590 min); log-rank test; P < 0.0001]. Sixty percent of HTEA patients were extubated within 30 min of the completion of surgery (in the operating room), compared with 5% of GA patients (Fig. 1). However, of those patients who remained intubated on arrival in the ICU, there were no differences in time to tracheal extubation: HTEA group, 458 min (230–594 min); GA group, 450 min (300–605 min). Within the HTEA group, patients extubated in the operating room were more likely to be male (97% vs 67%; P = 0.002) and to receive a smaller propofol dosage (median, 14.8 vs 17.6 mg/kg; P = 0.025).
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There was no difference in postoperative epinephrine and norepinephrine use (Table 2) between groups, although the GA group required more glyceryl trinitrate for vasodilation compared with the HTEA group (P = 0.02). The HTEA group had higher Paco2, lower lactate levels, and reduced postoperative SVR compared with the GA group (Table 3). HTEA patients tracheally extubated in the operating room had a higher Paco2 than HTEA patients extubated in the ICU (54 vs 48 mm Hg; P = 0.003).
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The cTnI levels were increased in both groups at 12 and 24 h, but there were no significant differences between groups (Table 4). The distribution of cTnI levels was not different in the two groups, and the nonparametric 95% confidence interval for the difference in median cTnI levels between groups was –2.1 to 2.4 µg/L. Eight (6.7%) patients developed new persistent Q waves by Day 5 (GA group, n = 5; HTEA group, n = 3). However, with combined ECG and cTnI criteria, only 3 (2.5%) patients had a transmural myocardial infarction (GA group, n = 2, HTEA group, n = 1) (Table 4). There was no difference between groups in the incidence of myocardial ischemia or infarction based on any of the following ECG or biochemical criteria: CK-MB% >8 at 12 and 24 h, Q wave and increased CK-MB%, ST increases, and cTnI or CK-MB increases.
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In the HTEA group, pain scores were significantly reduced compared with those in the GA group at all measurement times in the 72 h after surgery, both at rest and with coughing. The VAS results with coughing are shown in Figure 2. On average at rest, the VAS results were 28 mm less in the GA group and 9 mm less in the HTEA group compared with scores during coughing. In the GA group, the morphine dosage and duration of infusion (measured from the completion of surgery) were 46.5 mg (33–66 mg) and 41 h (33–51 h), respectively. Only the two patients with nonfunctioning epidurals required morphine in the HTEA group. The duration of epidural infusion was 70.5 h (67–73 h) at an average infusion rate of 8.1 mL/h, with median upper and lower limits of sensory block of C6 to T9 on Day 1, C7 to T6 on Day 2, and C8 to T6 on Day 3. Indomethacin was required in 25 GA patients and 24 HTEA patients; however, the median dosage in the GA group was 100 mg, compared with 200 mg in the HTEA group (P = 0.02). Oxycodone was required more frequently in the GA group (21 patients) compared with the HTEA group (9 patients). There were no differences in sedation or nausea scores between groups. Motor block in the upper limbs (mild hand weakness) occurred in 16% and 9% of patients on postoperative Days 1 and 2, respectively, and in all cases improved with reduction or temporary cessation of epidural infusion. There were no major complications due to epidural anesthesia or to other analgesic techniques.
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The HTEA group had one patient who required tracheal reintubation (for agitation) in the ICU. The GA group had two patients who required reintubation (one before reoperation for hemorrhage and one who required a tracheostomy for respiratory failure). There were two deaths in the GA group: one due to uncontrolled postoperative bleeding and one from postoperative stroke. There were no deaths in the HTEA group. There were no differences between the HTEA and GA groups in median total chest tube drainage (1460 vs 1510 mL, respectively), incidence of new postoperative atrial fibrillation (AF) (16 of 60 vs 20 of 60, respectively; P = 0.55), or median day of discharge [6.0 days (6–8 days) versus 6.5 days (6–8 days), respectively].
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this prospective randomized study, HTEA for elective CABG surgery had no effect on biochemical or ECG markers of myocardial ischemia or infarction. However, HTEA improved analgesia and facilitated earlier tracheal extubation.
cTnI is a sensitive and specific marker of perioperative myocardial infarction (12–15,18–20) and is an independent predictor of short- and long-term morbidity and mortality after CABG surgery (6,7). Reported levels of cTnI indicating perioperative myocardial infarction range from 11.6 to 40 µg/L (12–14,21), and although we used a threshold of 15 µg/L, our analysis showed no difference between groups regardless of the threshold used. A threshold of 15 µg/L at 24 hours would result in an incidence of infarction (Q or non-Q wave) of 32% and 33% in the HTEA and GA groups, respectively. This is consistent with the 30% incidence of non-Q wave infarction after CABG surgery found with sensitive tests such as technetium pyrophosphate scanning (22). Our sample size was adequate to exclude any clinically relevant difference in cTnI levels between groups, because the narrow 95% confidence intervals for cTnI indicate that any difference between groups would probably be <2.4 µg/L. Clearly this study was not powered to detect a difference in Q-wave infarction between groups; such a study would require several thousand patients.
The lack of an effect of HTEA on cTnI levels is in agreement with one study (8), but in contrast, Loick et al. (9) reported reduced troponin T release with HTEA. Differences between the study of Loick et al. and ours include fewer patients than this study, different cardioplegia techniques, different times to tracheal extubation, and a longer aortic cross-clamp period in our study (80 vs 49 minutes). Perhaps our infusion of ropivacaine 0.2% did not maintain a dense sympathetic block, compared with bupivacaine 0.75% in the study of Loick et al. However, Priestley et al. (8) used ropivacaine 1% and also found no effect on troponin levels with HTEA.
One limitation of our cTnI results is the more frequent prevalence of peripheral and cerebrovascular disease in the HTEA group. However, patients with and without these conditions had identical cTnI levels. Another potential limitation is that we measured cTnI only within 24 hours; therefore, we may have missed later events. However, a single 24-hour cTnI measurement has been shown to be reliable in detecting perioperative myocardial infarction (12) and predicting poor outcome (7). Despite the theoretical advantages of HTEA, factors such as technical difficulty in grafting and myocardial protection during the ischemic period may have a more significant effect than epidural anesthesia on troponin release.
Although the time to tracheal extubation in the HTEA group was significantly reduced, group allocation was not masked; therefore, bias toward early extubation in the HTEA group cannot be excluded (even though extubation criteria were standardized). A further limitation was a protocol requirement for reduced fentanyl dosage in the HTEA group, thus favoring earlier tracheal extubation. However, the investigators considered the prescribed fentanyl and morphine dosages necessary to facilitate hemodynamic stability and postoperative analgesia while retaining the capability to extubate early. Our finding of reduced extubation times with HTEA is in agreement with that of similar randomized controlled studies (1,8,9,11,23) with median extubation times ranging from 1.6 to 10 hours. It is important to note that nonepidural anesthesia techniques, such as remifentanil (24) and small-dose opioid (25,26) techniques, have been used to facilitate tracheal extubation in the operating room after off-pump surgery; however, these findings may not be applicable to on-pump CABG surgery with long CPB durations (as in our study).
Analgesia was improved in the HTEA group in the 72 hours after surgery, which is consistent with other reports (1,8,11). The longer duration of epidural infusion compared with that of the morphine infusion may have contributed to lower VAS scores on postoperative Days 2 and 3 in the HTEA group and increased oxycodone requirements in the GA group. However, it was decided to continue the existing unit practice and stop the morphine infusion on postoperative Day 2. The optimal duration of epidural analgesia after CABG surgery is not clear. Our decision to continue the infusion to postoperative Day 3 was strongly influenced by the general observation that post-CABG platelet counts were lowest on postoperative Days 1–2.
After anesthesia induction there were no significant hemodynamic differences between groups, except that poststernotomy MAP and SVR in the ICU were lower in the HTEA group. Apart from decreased postoperative glyceryl trinitrate use in the HTEA group, there was no significant difference in requirements for vasoactive drugs, which is consistent with other studies (27).
There was no difference in the incidence of AF between groups, consistent with two studies (8,28) but in contrast with a large study by Scott et al. (23), who found a significantly reduced incidence of AF with the use of HTEA. In the study of Scott et al., the epidural infusion included clonidine, which may have contributed to the less frequent incidence of AF.
There were no complications related to the epidural technique. The risk of epidural hematoma after epidural anesthesia in cardiac surgical patients has been estimated to be between 1 in 1,500 and 1 in 150,000 (29). This broad confidence interval is of limited value in our practice, where informed consent regarding risk is of paramount importance. There have been no case reports of epidural hematoma due to epidural anesthesia in fully anticoagulated patients having cardiac surgery. Heparin has no fibrinolytic effects, but cardiac surgery and CPB result in fibrinolysis and platelet dysfunction. Patients routinely received -aminocaproic acid during this study, but its contribution to the safety of neuraxial blockade in this population has not been determined. Inserting the epidural catheter the day before surgery was a conservative approach that has been the practice in most studies using HTEA for CABG surgery. However, admitting patients the day before surgery in a health care system in which day-of-surgery admission is routine may offset any economic advantage of earlier tracheal extubation. Although the combination of early tracheal extubation, cardiac sympathetic blockade, stress response attenuation, and excellent analgesia are unique to HTEA, its attendant complexity and potential for epidural hematoma cause its use to remain controversial.
In conclusion, in this study, the use of HTEA for CABG surgery had no effect on the release of cTnI as a marker of myocardial ischemia/infarction. However, HTEA improved postoperative analgesia and was associated with a reduced time to tracheal extubation.
The authors acknowledge the assistance of the staff of the Open Heart Surgical Unit and Intensive Care Unit and Dr. Simon McPherson, St. Vincent's Hospital, Melbourne.
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Footnotes |
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1 Martin B, Murphy F, Levy T, et al. Cardiac isoform of troponin-I (c-TnI): a sensitive marker of perioperative myocardial infarction (PMI) in CABG surgery [abstract]. Br J Anaesth 1999;82:A10.
This study received grants from the Australian Society of Anaesthetists and the Australian and New Zealand College of Anaesthetists.
Presented in part at the annual meeting of the Australian and New Zealand College of Anaesthetists, Brisbane, Australia, May 12, 2002, and at the Australian Society of Anaesthetists National Scientific Conference, Adelaide, Australia, October 26, 2002.
Accepted for publication September 14, 2004.
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