Use of epidural blockade in a patient with hip fracture and aortic stenosis

EDITOR: Patients with hip fracture are often frail and elderly, and co-morbidities are frequently present. The following case describes perioperative use of continuous epidural blockade in a patient with hip fracture and a severe aortic stenosis. This has not been reported before. There is no evidence favouring general anaesthesia to neuroaxial blockade in patients with aortic stenosis. Several case reports have shown that the use of epidural blockade for Caesarean section, labour and delivery in patients with aortic stenosis is safe [1-3]. A recently published article discussed the possibilities for using neuroaxial blockade in patients with aortic stenosis [4]. Case report An 80-yr-old female presented for surgery of a left-sided intracapsular hip fracture. She had a past medical history of stroke and 2 months earlier, cardiac arrest. The patient denied angina and dyspnoea. Her medications included citalopram, bendroflumethiazide with potassium chloride, oxazepam, paracetamol, simvastatin and ezetimibe. The physical examination revealed a Grade III-IV systolic murmur over the aorta with radiation to the neck. Electrocardiogram (ECG) showed sinus rhythm and a right bundle branch block. Echocardiography showed aortic stenosis and mitral insufficiency Grade I. The gradient across the aortic valve was estimated to 88-90 mmHg and the ejection fraction more than 60%. Preoperative blood tests were normal. On arrival in the emergency room a fascia iliaca compartment block was administered using 40 mL of bupivacaine 2.5 mg mL−1 with epinephrine 5 μg mL−1 as initial pain management. A lumbar epidural catheter was placed in the L2-L3 intervertebral space after 5 h and 40 min. Correct placement of the epidural catheter was tested with 3 mL of lidocaine 20 mg mL−1 and epinephrine 5 μg mL−1. This was followed by injection of 5 mL bupivacaine 2.5 mg mL−1 supplemented with another 5 mL bupivacaine 2.5 mg mL−1 after 45 min resulting in subjective analgesia and a T10 sensory level. Subsequently, a continuous infusion with 4 mL h−1 of bupivacaine 0.125 mg mL−1 and morphine 50 μg mL−1 was started. Prior to the neural blockade a total of saline 0.18%/glucose 5% 1000 mL was given intravenously (i.v.), followed by saline 0.9% 500 mL. Blood pressure (BP) fell from 160/90 to 120/70 and then remained stable. Heart rate (HR) was 70-75 bpm throughout the procedure. Before surgery the following day the patient's BP was 120/50 with HR of 65 bpm. Supplementary oxygen (O2) therapy was administered via nasal cannulae and routine monitoring was applied including three lead ECG, pulse oximetry and non-invasive BP. The continuous epidural infusion was paused and 25 mg ephedrine was administered intramuscularly (i.m.) and 15 mg of bupivacaine with 1 mg morphine was injected into the epidural catheter. The initial bupivacaine dose of 15 mg was repeated after 35 min resulting in a T10 sensory level and surgery commenced. During surgery saline 0.9% 1000 mL and 500 mL hetastarch 130/0.4 was administered i.v. to maintain preload. Intraoperatively a supplemental bupivacaine dose of 15 mg was repeated 55 and 95 min after the initial dose. BP and HR remained unchanged during surgery. Blood loss was estimated at 800 mL. The recovery period was uneventful. Blood loss was replaced with 2 × 300 mL erythrocyte suspensions. As soon as the patient was able to perform normal knee flexion of the unaffected leg, the continuous epidural infusion was resumed and the patient was discharged after 2 h. Postoperative analgesia was maintained for 4 days using the epidural infusion with bupivacaine 0.125 mg mL−1 and morphine 50 μg mL−1. The patient recovered without sequelae and was discharged home after 14 days of rehabilitation. Six months after discharge the patient was alive and well. Discussion There are no evidence-based recommendations for the best choice of anaesthesia and postoperative analgesia in the patient with aortic stenosis. At Hvidovre University Hospital perioperative continuous epidural blockade is used as a part of a multimodal intervention in a fast track regimen in patients with hip fracture. Neuraxial blockade potentially reduces mortality and other serious complications in lower extremity surgery [5]. Preoperative administration of epidural analgesia compared to opioid analgesia provides a reduction in cardiac events and pain in patients with hip fracture and cardiac co-morbidities [6]. Pain and the resulting tachycardia may have deleterious haemodynamic consequences in the patient with aortic stenosis as recently mentioned by McDonald [4]. There is ample evidence to show that epidural analgesia provides better postoperative analgesia compared to parental opioid analgesia [7]. Furthermore, it has been demonstrated that postoperative epidural analgesia, probably because of superior pain management, reduces the amount of cardiac ischaemia in patients with hip fracture [8]. In major knee surgery it has been demonstrated that earlier rehabilitation can be achieved by using epidural blockade in contrast to i.v. patient controlled morphine [9]. This may also be possible in patients with hip fracture, and therefore requires further evaluation. When anaesthetizing a patient with aortic stenosis, the haemodynamic goals include avoiding sudden and profound decreases in systemic vascular resistance, maintaining contractility and sinus rhythm and avoiding hypovolaemia and tachycardia [4]. Epidural blockade facilitate a gradual unset of anaesthesia and sympathetic block, and therefore a sudden and profound decrease in systemic vascular resistance is avoided. With incremental doses of local anaesthetics, an even higher degree of control is attained. Epidural anaesthesia does not affect cardiac contractility and with volume loading, preload can be maintained. Epidural anaesthesia provides several evidence-based advantages in the patient with hip fracture, which is why we chose it for our patient. It must be emphasized that the choice of anaesthesia must be evaluated in each case, especially in patients with aortic stenosis, based on knowledge of pathophysiology and haemodynamic goals. Acknowledgements This work received financial support from Apotekerfonden af 1991, IMK fonden and The Danish Research Council (No. 22-01-0160). M. Bundgaard-Nielsen N. B. Foss B. B.