High thoracic epidural analgesia for cardiac surgery: an audit of 874 cases.
Despite clinical use for over 10 years, high thoracic epidural analgesia for cardiac surgery remains controversial, due to a perceived increased risk of epidural haematoma resulting from anticoagulation for cardiac pulmonary bypass. There are no sufficiently large randomised studies to address this question and few large case series reported. For this reason, we conducted an audit of neurological complications related to high thoracic epidural analgesia during cardiac surgery in our institution between 1998 and end 2005. During this period 874 patients received epidural analgesia. There were no neurological complications attributable to epidural use. Our findings suggest that major neurological complications related to high thoracic epidural use during cardiac surgery are rare.
Key Words: epidural, analgesia, cardiac surgery, audit
The use of high thoracic epidural analgesia for cardiac surgery remains controversial despite clinical use for over 10 years (1-3). The predominant concern relates to the possibility of an increased risk of epidural haematoma associated with anticoagulation during cardiac surgery. There are no randomised trials sufficiently powered to answer this question and few large case series reported. In the absence of large randomised trials, it is important to identify how many epidurals have been reported and how many complications have occurred, in order to identify whether epidural use in cardiac surgery is associated with similar risk compared with use in non-cardiac surgery.
The aim of this audit was to determine the incidence of neurological complications in our case series.
We conducted a retrospective audit of high thoracic epidural (HTEA) use in cardiac surgery from 1998 until end 2005. The Human Research Ethics Committee of Melbourne Health approved the study as an audit project. Although we first started performing epidurals in mid-1997, the custom cardiothoracic surgery database used in this audit was not started until 1998. All patients who had received HTEA for cardiac surgery (including off-pump coronary artery bypass graft surgery (CABG)) in this time period and recorded on the database were included. Patients receiving HTEA for thoracic surgery were not included.
Patients were placed in the sitting position and an epidural needle inserted at the T1/2, T2/3, or T3/4 interspaces. The catheter was inserted, aiming to leave 3 to 5 cm within the epidural space. A loading dose of 35 to 50 mg ropivacaine (0.5%) was administered prior to induction of anaesthesia and thereafter an infusion of local anaesthetic with supplemental opiate was continued into the postoperative period. Contraindications to HTEA included patient refusal, abnormal coagulation (INR >13), systemic anticoagulation (any unfractionated heparin <6 hours, low molecular weight heparin <24 hours, clopidogrel <7 days, ticlopidine <2 weeks, or GPIIb/IIIa inhibitors <7 days), any active or increased risk of infection or sepsis, any spinal abnormality, or previous surgery or trauma to the spine from the neck to the mid-thoracic region. Following catheter insertion, the minimum period from insertion to anticoagulation was one hour.
The technique has evolved from insertion of the epidural on the day prior to surgery since 1997 to the day of surgery in 2000. The methods, efficacy and outcome of this technique are described in a previous randomised controlled trial (4). All patients received general anaesthesia for surgery in addition to the HTEA. We found that the use of epidural morphine (20 [micro]g/ml) rather than fentanyl (2 [micro]g/ml) as the opiate adjunct to 0.2% ropivacaine resulted in fewer patients experiencing breakthrough pain and allowed a lower rate of infusion to achieve adequate analgesia (5).
Anticoagulation for cardiopulmonary bypass consisted of an initial dose of heparin of 300 [U.kg.sup.-1], aiming to attain a minimal activated clotting time (ACT) of 400 s. Repeated doses of heparin were administered as required to maintain the ACT > 400 s. For off-pump cardiac surgery, an initial dose of 100 [U.kg.sup.-1] heparin was administered, aiming for a minimal ACT >200 s. Following the coronary artery grafting and/or weaning from CPB, the heparin was reversed with protamine 1 [mg.kg.sup.-1] for off-pump cases and 3 [mg.[kg.sup.-1] for CPB cases. Subcutaneous heparin (5000 U tds) or enoxaparin (40 mg bd), was administered following surgery until the patients were ambulant. Prior to epidural removal, the dose was withheld and was administered two hours following epidural removal.
Postoperative epidural management
The epidurals were managed by the pain management service and patients were reviewed at least daily. Neurological complications, whether they were thought to be surgery-related or epidural-related, were referred to a neurologist for opinion and management. Specifically, signs or symptoms relating to possible haematoma included back pain, bilateral limb weakness (particularly of the lower limbs), or any sensory loss of the lower limbs at any time, or of the upper limbs persisting several hours after cessation of the epidural. The audit only encompassed neurological issues related to central neuraxial blockade.
Patient demographic variables and operative details are shown in Tables 1 and 2. The majority of cases were CABG, reflecting the caseload of our unit during this time period.
There were no neurological complications related to central neuraxial blockade in any of the patients reported. There were approximately 30 patients where epidurals were performed prior to inclusion on the database, without epidural related neurological complications. The data cut-off for data accrual was December 2005 and there have not been any epidural related neurological complications subsequent to that date.
One patient who had undergone extensive aortic arch surgery developed progressive paralysis of the legs 24 hours after surgery. The surgery had involved placing a long endovascular stent to cover the arch and proximal descending aorta, and the patient had previously undergone abdominal aortic replacement. At the time, the patient had become mildly hypotensive and with the institution of vasopressor support (noradrenaline), there was a rapid reversal of paralysis (within 20 minutes). Deliberate hypertension was maintained for 24 hours and there was complete recovery. Expert neurologist opinion was sought and it was considered that the relative hypotension in the setting of extensive surgical disruption to thoracic and abdominal spinal cord collateral blood supply resulted in temporary spinal cord hypoperfusion. The rapid reversal of neurological symptoms with increased blood pressure confirmed the diagnosis and spinal imaging was not performed.
HTEA has been shown to be highly effective in providing excellent analgesia for patients undergoing cardiac surgery (2,4,6-8). The key reported advantages of HTEA relate to improved analgesia, physiotherapy cooperation, improved lung function, early extubation, reduced arrhythmia and reduction in troponin T levels, as well as reduced psychological morbidity (4,8-10) None of the current studies, however, is adequately powered to detect an outcome difference in patients undergoing cardiac surgery.
Despite the use of HTEA in cardiac surgery for more than 10 years, there is still considerable controversy surrounding its use (3). The controversy does not relate to whether HTEA can provide optimal analgesia, but rather surrounds the fear of neurological injury and, specifically, whether the incidence of neurological injury is increased in patients who are concomitantly anticoagulated during cardiac surgery. The question of risk versus benefit can only properly be addressed by a very large randomised trial, which is unlikely to be performed because of the low incidence of neurological injury (3). Safety may be indirectly assessed by knowing the incidence of neurological injury and the denominator (the number of epidurals performed). Although an estimate of case numbers has been provided in recent articles (3,11), the true number of epidurals used in cardiac surgery is not known.
There has been one published case of epidural haematoma that followed the administration of thrombolytic therapy and an indirect report in a recent review article of two further cases that were cited as "personal knowledge" by the author of that article (3). Full details of those cases cannot be evaluated unless and until they are published.
Our primary aim was to determine our incidence so as to add to the body of knowledge in this area. Neurological injury does occur with epidural use and it is not logical to think that neurological injury will never occur in cardiac surgery. However, it is important to identify whether the risk is increased in patients receiving systemic anticoagulation for cardiac surgery compared with epidural use in general. There is no evidence to date that there is increased risk associated with use of epidurals in cardiac surgery compared with other forms of surgery. In other fields of surgery or during labour, the use of epidural anaesthesia and analgesia is well established with an identified and accepted risk of major complication. It is the acceptance of a reasonable level of risk that has not been established in cardiac surgery to date. In contrast, cerebral neurological injury in cardiac surgery is very common with a risk of stroke or coma of 1 to 5% and the potential risk of lesser though still disabling neurocognitive decline of 20 to 50% (12-14).
This report alone is insufficient to provide safety data but, when added to the world literature, will allow the clinician to better judge safety. In 2003, Gravlee (15) cited more than 6000 cases of HTEA in cardiac surgery without neurological complication attributable to the epidural. Since then, two other large case series and including this report have added a further 5824 cases without epidural-related spinal damage (6,16). This is likely to be a significant underreporting of the number of cases actually performed, though it is also equally possible that cases of epidural related neurological damage are under-reported. In a recent meta-analysis, Ruppen et al (17) evaluated 5026 patients who underwent vascular surgery, 4971 cardiac surgery and 4108 thoracic surgery with epidural analgesia. There was no case of permanent spinal damage and their zero-incidence analysis of the "worst-case" risk for catastrophic neurological damage was 1:1700 for cardiac surgery, 1:1400 for thoracic and 1:1700 for vascular surgery. In this case series, the zero-incidence analysis is a risk of spinal damage from 0 to 1:291 cases, but when added to the world literature, the zero-incidence risk is 0 to 1:4000. These data and analyses suggest that the risk for epidural use in cardiac surgery is unlikely to be different from its use in non-cardiac surgery.
The limitation of the report is that it is an audit rather than a randomised prospective trial or prospectively acquired observational study. We do not have the level of detail to report all neurological complications associated with cardiac surgery in this cohort and so have restricted our report to neurological complications associated with the use of epidural analgesia. Our data is intended to add to the body of the existing literature rather than to make direct inferences of safety from this data set. Our findings suggest that incidence of symptomatic epidural haematoma leading to neurological complications following HTEA use in cardiac surgery is rare.
We thank our colleagues and nursing staff who assisted with our epidural program.
Accepted for publication on January 4, 2007.
(1.) Liem TH, Booij LH, Hasenbos MA, Gielen MJ. Coronary artery bypass grafting using two different anesthetic techniques: Part I: Hemodynamic results. J Cardiothorac Vasc Anesth 1992; 6:148-155.
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C. F. ROYSE *, P.F. SOEDING ([dagger]), A. G. ROYSE ([double dagger])
Departments of Anaesthesia and Pain Medicine and Cardiothoracic Surgery, Royal Melbourne Hospital and Department of
Pharmacology, University of Melbourne, Melbourne, Victoria, Australia
* M.B., B.S., M.D., F.A.N.Z.C.A., Associate Professor, Anaesthesia and Pain Management Unit, Department of Pharmacology, University of Melbourne and Department of Anaesthesia and Pain Medicine, Royal Melbourne Hospital.
([dagger]) M.B., B.S., F.A.N.Z.C.A., Consultant Anaesthetist, Department of Anaesthesia and Pain Medicine, The Royal Melbourne Hospital and Cardiovascular Therapeutics Unit, Department of Pharmacology, University of Melbourne.
([double dagger]) M.B., B.S., M.D., F.R.A.C.S., Associate Professor, Cardiovascular Therapeutics Unit, Department of Pharmacology, University of Melbourne and Department of Cardiothoracic Surgery, Royal Melbourne Hospital.
Address for reprints: A/Prof C. Royse, Anaesthesia and Pain Management Unit, Department of Pharmacology, Level 8 Medical Sciences Building, University of Melbourne, Carlton, Vic. 3010.
TABLE 1 Demographic details for 874 patients Variable Mean Standard deviation Age 69.4 10.6 Height (cm) 165.1 20.1 Weight (kg) 78.2 16.9 Body mass index ([kg.[m.sup.2]]) 28.4 4.9 Variable n % Male gender 633 72.4 Hypertension 378 43.2 Diabetes 228 26.1 Smoker--never 430 49.2 Smoker--ceased 377 43.1 Smoker--current 67 7.7 Previous AMI 279 31.9 AMI is acute myocardial infarction. TABLE 2 Operative details Variable Mean Standard deviation CPB time (min) 103.4 53.2 X-clamp time (min) 77.5 42.6 Number of distal anastomoses 2.6 1.6 Variable n % OPCABG 162 18.5 CABG--total 632 72.3 CABG+valve 88 10.1 Valve 121 13.8 Aortic 12 1.4 Thoracic req CPB 21 2.4 CPB is cardiopulmonary bypass; X-clamp is cross-clamp; number of distal anastomoses refers to CABG cases only. OPCABG is off pump coronary artery bypass graft surgery and refers to coronary artery surgery performed without the aid of cardiopulmonary bypass; CABG includes the OPCABG cases; valve is any valve repair or replacement; aortic is any aortic surgery whether or not valve replacement is included, thoracic req CPB is the thoracic or mediastinal operation requiring cardiopulmonary bypass (for example mediastinal tumour resection involving great vessels).
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|Author:||Royse, C.F; Soeding, P.F.; Royse, A.G.|
|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Clinical report|
|Date:||Jun 1, 2007|
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