Surgery for dysphagia lusoria caused by right aberrant subclavian artery: Anesthesia perspective

Surgery for Dysphagia Lusoria Caused by Right Aberrant Subclavian Artery: Anesthesia Perspective Shrinivas Vitthal Gadhinglajkar, MD, Rupa Sreedhar, MD, Madathipat Unnikrishnan, MCh, and Ravi Varma, MD

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YSPHAGIA LUSORIA occurs because of an aberrant right subclavian artery, which passes behind the esophagus. Many reports are available in the literature regarding its surgical treatment.1-3 However, there is no report, to the authors’ knowledge, that describes anesthesia management during the surgical procedure for this anomaly. This case report will focus on the most important aspects of the anesthetic management of patients with dysphagia lusoria. CASE REPORT A 52-year-old woman was admitted to the hospital with gradually progressing dysphagia of 2 years’ duration. She had difficulty in swallowing liquids the last 2 months. There were no symptoms of tracheal compression. She was a known hypertensive for the last 7 years and was on 5 mg of oral amlodipine per day. Her blood pressure was almost equal in the right and left arms. Allen’s test performed by occluding the radial artery suggested patency of collateral circulation in both hands. An aortogram revealed a right aberrant subclavian artery (aSA) originating from the aorta as its last branch distal to the origin of the left subclavian artery and later on taking a tortuous course toward the right (Fig 1). Barium meal along with selective injection of the right aSA showed an indentation of the midesophagus with transient holdup of barium proximal to it (Fig 2). Left ventricular function was normal on echocardiography. A treadmill test was negative for inducible ischemia. The patient was posted for surgery via right thoracotomy. Premedication included oral diazepam, 7.5 mg, on the previous night and in the morning on the day of surgery. She received her morning dose of amlodipine, 5 mg. She also received an intramuscular injection of glycopyrrolate, 0.2 mg, 1 hour before surgery. After arrival in the operating room, an 18-G epidural catheter (Perifix; B/Braun, Melsungen, Germany) was introduced by the midline approach between the fourth and fifth thoracic vertebrae with the patient in the sitting position. Proper placement was tested with 3 mL of lidocaine, 10 mg/mL. A 20-G catheter was inserted in the left radial artery under local anesthesia for invasive pressure monitoring. Anesthesia was induced intravenously with midazolam, 2.5 mg, fentanyl, 200 ␮g, and sodium thiopental, 250 mg. Muscle relaxation was accomplished with pancuronium bromide, 8 mg. Lidocaine, 75 mg, was injected intravenously 90 seconds before the trachea was intubated with a number 35F left-sided double-lumen endobronchial tube (Bronchocath; Mallinckrodt Medical, Dublin, Ireland). The authors assessed correct placement of the endobronchial tube by auscultation as well as by fiberoptic bronchoscopy. Anesthesia was maintained with isoflurane, oxygen, and nitrous oxide. Fentanyl was supplemented as needed. A triple-lumen cannula (Certofix, B/Braun) was introduced into the right internal jugular vein. The authors also cannulated the right radial artery for invasive pressure monitoring. The pressures in the left and

From the Department of Anesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India. Address reprint requests to Shrinivas Vitthal Gadhinglajkar, Department of Anesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India 695011. E-mail: shri@ sctimst.ker.nic.in © 2005 Elsevier Inc. All rights reserved. 1053-0770/05/1901-0017$30.00/0 doi:10.1053/j.jvca.2004.11.017 Key words: dysphagia lusoria, subclavian artery 86

right radial arteries were 122/88 mmHg and 120/86 mmHg, respectively. Epidural anesthesia was begun with a bolus injection of 10 mL of bupivacaine, 5 mg/mL. Subsequently, the patient received a continuous infusion of bupivacaine (2.5 mg/mL) and fentanyl (10 ␮g/mL) at the rate of 4 to 8 mL/h. The patient had an episode of bradycardia and hypotension 45 minutes after bolus epidural injection, which responded to injection of atropine, 0.6 mg, and phenylephrine, 3 ␮g/kg. Monitoring included invasive blood pressure, electrocardiography, central venous pressure, pulse oximetry, capnometry, urine output, and measurement of core temperature. The authors monitored the pulsations of the right radial artery and changes in forearm temperature. The aberrant right subclavian artery was accessed through the right thoracotomy. One-lung ventilation was instituted after the opening of the pleura. The right aSA was posterior to the esophagus, which was dissected out proximally after placing a tape carefully around the esophagus. It was compressing the esophagus without compression of the trachea. Test clamping of the vessel resulted in the loss of the pulsatile pattern on the monitor displaying invasive blood pressure in the right radial artery and also the loss of the pulse oximeter signal in the right hand. After administration of systemic heparin, 1 mg/kg, and attaining an activated coagulation time of 205 seconds, the aberrant artery was divided between clamps as far to the left side of the esophagus as possible. An 8-mm Dacron graft was sutured end-to-end to the right aSA. The other end of the graft was sutured end-to-side to the ascending aorta after applying a partial occlusion clamp on the aorta, establishing antegrade flow through the right subclavian artery. The perfusion pressure was about 60 to 70 mmHg in the right radial artery as long as the right aSA remained clamped. The temperature of the right hand did not change significantly during that period. The mean pressures in the left radial artery were maintained at about 90 mmHg. Pressures became equal in both radial arteries after releasing the clamps on the aorta and right subclavian artery. Arterial blood gases were well maintained throughout surgery. Heparin was reversed with protamine, and dual-lung ventilation was reestablished. The total duration of 1-lung ventilation was about 2 hours. The neuromuscular blockade was reversed with neostigmine and glycopyrrolate at the end of surgery. The trachea was extubated. Epidural infusion of bupivacaine and fentanyl was continued in the postoperative period for 64 hours. The level of sensory block was tested after extubation. It extended from the level of T1 to T10 sensory spinal segments. Both radial artery pressures were equal, and the right hand remained warm. There were no syncopal attacks in the early postoperative period. There was complete relief from dysphagia. The Doppler ultrasonographic examination showed good forward flow in implanted vessel and graft. There was antegrade flow in the vertebral artery (Fig 3). The patient was discharged with advice to continue oral amlodipine (5 mg/d) and aspirin (75 mg/d). She was symptom free when she came for review 3 months and 2 years after surgery. A computed tomography scan with 3-dimensional reconstruction of the image performed during review showed implantation of the subclavian artery on the ascending aorta (Fig 4). DISCUSSION

The aSA is the most frequently encountered anomaly of the aortic arch, and it is found in approximately 0.5% of normal individuals.1 In patients with dysphagia lusoria, the diagnosis of right aSA is made by a barium meal study, which shows a typical posterior oblique indentation in the barium-filled esophagus near the third or fourth thoracic vertebra.2,3 However, for an accurate visualization of aSA and its relation to the neigh-

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Fig 3. Color Doppler image of the neck vessels showing antegrade flow pattern in the right vertebral artery similar to that of the right common carotid artery.

boring organs, an aortogram is indicated.4 The aortogram reveals right aSA arising at the fourth branch of the arch.5 Bicarotid truncus can be found in 29% of patients having right

aSA, and in these patients, symptoms of esophageal compression are more severe.3 The aortogram can be combined with a barium meal under cinefluoroscopy, showing the compression of the esophagus by the pulsating right aSA. Although right aSA is a congenital anomaly, in most of the cases it is asymptomatic until middle age. Dysphagia lusoria generally develops during the fourth decade of life. Elongation of arteries, a high aortic arch caused by aging, and hypertension are possible ways of explaining the late onset of dysphagia.1 The present patient became hypertensive in the fifth decade of life. Symptomatic patients require surgical intervention. Kieffer et al1 reported aneurysm of the aSA in 10 of 33 patients. Aneurysm of the aSA, whether it is symptomatic or not, is an indication for surgery.1

Fig 2. Selective angiogram of right aberrant subclavian artery with simultaneous barium esophagogram showing interruption of the barium column.

Fig 4. Three-dimensional shaded surface display reconstructed image of the aortic arch showing the right subclavian artery reimplanted on the aortic arch through the interposition graft.

Fig 1. Arch aortogram showing aberrant origin of right subclavian artery distal to the origin of left subclavian artery.

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Various approaches have been described in the literature for the definitive surgical treatment of dysphagia lusoria. The aSA can be transected behind the esophagus and reimplanted on the ascending aorta via right thoracotomy in a single operation.6 Other approaches include midline sternotomy,2 left posterolateral thoracotomy,3 median cervicosternotomy, isolated cervicotomy, and cervicotomy associated with contralateral thoracotomy.1 Cardiopulmonary bypass may be needed for patients with aneurysmal aberrant subclavian artery or when there is an associated lesion such as ascending aortic aneurysm or ventricular septal defect. Division of aSA without reestablishment of arterial continuity can lead to ischemic complications either in the upper limb or in the vertebrobasilar territory. Reversal of flow from the vertebral artery to the distal subclavian artery may occur when there is obstruction in the first part of the subclavian artery that can produce vertebrosubclavian steal.5 Such reversal may occur when the first part of the subclavian artery is ligated. To prevent ischemia of the upper limb and vertebrosubclavian steal, axilloaxillary bypass can be performed3 or the right aberrant subclavian artery can be anastomosed either to the right carotid artery or the ascending aorta.4 Repeated pulmonary infections may occur because of dysphagia in children. Pediatric patients may present with respiratory symptoms like dyspnea, cough, and noisy breathing. Dysphagia as a result of aSA in adults is most often isolated, without associated respiratory disorder caused by tracheal compression. Right aSA usually (80%) traverses behind the esophagus. Sometimes (15%) it passes between the esophagus and the trachea and rarely (5%) in front of the trachea,3 and these patients may have predominant respiratory symptoms. Large space– occupying aneurysms of right aSA may be the cause of tracheal compression in adult patients. All patients having respiratory symptoms and aneurysm of the right aSA should undergo bronchoscopy to locate the site of tracheal compression and to rule out presence of tracheomalacia. Bronchoscopy shows excessive pulsations over the posterior aspect of the trachea produced by the right aSA traversing the same area.5 The trachea should be intubated carefully if right aSA is aneurysmal, so as to avoid its rupture. Lung isolation and 1-lung ventilation using a double-lumen tube not only improves surgical exposure but also protects the nondependent lung from the trauma of surgical retraction. The left radial artery should be cannulated for dedicated invasive pressure monitoring throughout the surgery. Cannulation of the right radial artery (in addition to cannulation of the left radial artery) helps in many ways. Firstly, temporarily occluding the vessel and observing changes in the right radial artery waveform can identify the right aSA. Secondly, right radial artery pressure reflects the adequacy of blood flow to the right upper limb, after reimplantation of the transected vessel on the ascending aorta or carotid artery. Finally, right radial artery pressure of 90 to 100 mmHg systolic after division of the right aSA suggests that perfusion of the right upper limb would be adequate in the early postoperative period if the surgeon decides to only ligate (with or without division) the aSA in a patient with a diseased aorta and carotid artery. There is a possibility of inadequate cerebral perfusion during

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anastomosis of the right aSA to right carotid artery because there will be interruption of blood flow in the right carotid artery as well as the right vertebral artery for a brief period. Cerebral protective strategies should be instituted to prevent neurologic damage during this period of possible cerebral ischemia. A test clamping of the right carotid artery could be performed to assess the ipsilateral cerebral perfusion using stump pressure measurement or measurement of blood flow velocity in the right middle cerebral artery by transcranial Doppler. If the stump pressure measured above the clamped area is more than 60 mmHg, active measures are not needed to protect the brain. If mean flow velocity in the middle cerebral artery (MCA) by transcranial Doppler is more than 40% of preclamp value,7 cerebral ischemia is absent. Electroencephalographic monitoring is also a useful method of assessing the risk of cerebral ischemia during carotid endarterectomy.8,9 However, if the stump pressure measurement or MCA blood flow velocity are less than the previously mentioned figures or if an electroencephalogram shows changes of ischemia, the brain needs to be protected. The insertion of a shunt across the clamped carotid artery; mild systemic hypothermia; induced hypertension; and administration of low-dose sodium thiopental (3-5 mg/kg), mannitol 1 g/kg, dexamethasone, 0.5 mg/kg, may be considered for this purpose. The patient should be ventilated with 100% oxygen during the clamping of the carotid artery. Adequate venous access should be established because major bleeding can be anticipated during surgery. Epidural analgesia administered in addition to general anesthesia reduces perioperative stress, possibility of myocardial ischemia, and postoperative pain. It facilitates early extubation and mobilization of the patient.10 A thoracic epidural catheter can be placed before induction of anesthesia,11,12 as was done in the present patient. This enabled the authors to know the extent to which the sensory and autonomic blockade could be achieved with the spread of epidural infusion of local anesthetic. Ten milliliters of bupivacaine in the concentration of 5 mg/mL injected at T5 (interstitium) will at least result in a T1-T12 (sensory segmental) block, leading to a potent sympathetic block.13 The authors could achieve epidural block up to T1-T9 (sensory segments) even though bupivacaine was used in the concentration of 2.5 mg/mL. In addition to providing postoperative pain relief, the sympatholytic effect of epidural bupivacaine may facilitate maintenance of forward flow in the subclavian artery because of its sympatholytic effect. High thoracic epidural block has been reported to increase vascular diameter and blood flow in the common carotid artery.14 Magnusdottir and associates15 found that skin temperature significantly increased in the hands of patients after injection of bupivacaine in the thoracic epidural space. Similar observations indicating sympatholytic effect of thoracic epidural block has been noted by others.16 Continuous epidural analgesia in the heparinized vascular surgical patients is safe and outweighs theoretic contraindications when anticoagulation is planned as part of an operative event.17 Odoom and Sih18 inserted an epidural catheter in 950 vascular surgical patients who were on anticoagulant drugs preoperatively. All patients received intraarterial injections of heparin before arterial cross-clamp. None of their patients developed any neurologic complications during their stay in the hospital.

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In summary, the division of the right aberrant subclavian artery is the definitive way of relieving dysphagia lusoria. The divided right aberrant subclavian artery needs to be reimplanted to prevent ischemia of the right upper limb and vertebrosubclavian steal. General anesthesia combined with thoracic epidural anesthesia provides hemodynamic stability. One-lung

anesthesia facilitates surgical dissection. Invasive monitoring of blood pressure in both radial arteries helps in operative decisions. Infusion of thoracic epidural local anesthetics not only imparts postoperative pain relief but also induces vasodilatation by sympatholysis, which augments forward blood flow in the implanted subclavian artery.

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Effects on ventilation-perfusion relationships. J Cardiothorac Vasc Anesth 13:258-264, 1999 11. Kasaba T, Kondou O, Yoshimura Y, et al: Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia. Can J Anaesth 45:1061-1065, 1998 12. Brodner G, Pogatzki E, Van Aken H, et al: A multimodal approach to control postoperative pathophysiology and rehabilitation in patients undergoing abdominothoracic esophagectomy. Anesth Analg 86:228-234, 1998 13. Stenseth R, Berg EM, Bjella L, et al: Effects of thoracic epidural analgesia on coronary hemodynamics and myocardial metabolism in coronary artery bypass surgery. J Cardiothorac Vasc Anesth 9:503-509, 1995 14. Murakawa K, Noma K, Ishida K, et al: Circulatory effects of stellate ganglion block and high thoracic epidural block. Masui 43:9981003, 1994 15. Magnusdottir H, Kirno K, Ricksten S, et al: High thoracic epidural anesthesia does not inhibit sympathetic nerve activity in the lower extremities. Anesthesiology 91:1299-1304, 1999 16. Satoh K, Ohe Y, Kobayashi N, et al: Relation between fingertip temperature pattern and epidural puncture site during epidural anesthesia combined with general anesthesia. Masui 42:60-65, 1993 17. Baron HC, LaRaja RD, Rossi G, et al: Continuous epidural analgesia in the heparinized vascular surgical patient: A retrospective review of 912 patients. J Vasc Surg 6:144-146, 1987 18. Odoom JA, Sih IL: Epidural analgesia and anticoagulant therapy. Anaesthesia 38:254-259, 1983