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CARDIOVASCULAR ANESTHESIA

Bilateral Vocal Cord Palsy During Carotid Endarterectomy Under Cervical Plexus Block

Angel O. K. Kwok, FHKAM (Anaesthesiology), FANZCA^*, Brendan S. Silbert, FANZCA, Kara J. Allen, MBBS, Peter J. Bray, MBBS, and John Vidovich, FRACS¹

*Department of Anaesthesiology and Operating Theatre Services, Kwong Wah Hospital, Kowloon, Hong Kong, China; and Departments of Vascular Surgery and Anaesthesia, St. Vincent’s Hospital, Melbourne, Australia

Address correspondence to Brendan Silbert, FANZCA, Department of Anaesthesia, St. Vincent’s Hospital, PO Box 2900, Fitzroy, Australia 3065. Address e-mail to silberbs{at}svhm.org.au.

	Abstract

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We describe a case of vocal cord palsy leading to respiratory obstruction during carotid endarterectomy under cervical plexus block in a patient who had preexisting contralateral vocal cord paralysis subsequent to a previous thyroidectomy. The patient required immediate tracheal intubation and subsequent tracheostomy to maintain the airway postoperatively. Care must be given to avoid contralateral vocal cord paralysis in the presence of a preexisting vocal cord palsy.

	Introduction

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Carotid endarterectomy (CEA) under cervical plexus block has several advantages, including awake neurological assessment (1); however, cranial nerve injury may occur as a result of the block or surgery (2). We report a patient who underwent CEA under cervical plexus block who we suspect had suffered contralateral vocal cord palsy during a prior thyroidectomy and who now experienced an ipsilateral vocal cord palsy resulting in respiratory obstruction.

	Case Report

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A 65 kg, 70-yr-old woman was admitted for left CEA. She had undergone thyroidectomy 15 yr previously. Neurological examination was normal, and she had no stridor or hoarseness.

An IV infusion of lactated Ringer’s solution 1000 mL was commenced, oxygen administered, and routine monitoring established (electrocardiogram, pulse oximetry, intraarterial blood pressure). Midazolam (1 mg) and dexmedetomidine (initial dose 0.5 µg/kg over 10 min, followed by infusion at 0.2 µg·kg^–1·h^–1) was used for sedation. Deep and superficial cervical plexus blocks were performed using 1.5% lidocaine with 1;200,000 epinephrine (3). Six mL was injected at C3, C4, and C5 and 12 mL was injected into the superficial plexus.

The common carotid artery (CCA) was exposed and the vagus nerve was identified. A Pilling retractor was introduced to retract the internal jugular vein and sternocleidomastoid laterally and thyroid and trachea medially. When the plane medial to the CCA was opened, the patient coughed repeatedly. This was interpreted as discomfort and 2 mL of plain lidocaine (1%) was infiltrated around the CCA. The patient then developed stridor and became agitated so the retractor was removed. The respiratory distress resolved and she was able to communicate normally after 2 min, although her voice was noted to be hoarse. On replacing the retractor the patient again developed cough and stridor immediately, which this time did not resolve when the retractor was removed.

General anesthesia was then induced 45 min after the commencement of surgery with fentanyl 100 µg, propofol 120 mg, and rocuronium 50 mg, and the trachea was intubated. Anesthesia was maintained with oxygen-air-sevoflurane and the surgery continued for a further 75 min. The distal internal carotid artery was inspected for test clamping but was found to have a solid posterior plaque extending behind the angle of the mandible, inaccessible to surgery. Carotid stenting at a later date was deemed to be the most appropriate treatment. The vagus nerve was inspected and found to be intact. The patient did not have a nonrecurrent laryngeal nerve, and the recurrent laryngeal nerve was not exposed.

To assess the vocal cord mobility, the patient was allowed to spontaneously breathe sevoflurane after reversal of the muscle relaxation; the trachea was then extubated and a size #3 laryngeal mask airway inserted. Fiberoptic bronchoscopic (FOB) assessment with the patient breathing spontaneously showed bilateral vocal cord adduction with moderate supraglottic edema (Fig. 1). We consulted an ear-nose-throat surgeon. Although reintubating the trachea and ventilating the patient’s lungs in intensive care overnight was an option, it was the opinion of the ENT surgeon that tracheostomy would be a more suitable alternative, especially in view of the associated cord edema. Tracheostomy was performed under general anesthesia and the patient made an uneventful recovery.

View larger version (131K): [in this window] [in a new window]   Figure 1. Bronchoscopic assessment immediately after surgery showing bilateral vocal cord palsy and supraglottic edema.

Serial FOB assessment was performed on days 2, 5, and 9 after tracheostomy. Bilateral vocal cord paralysis and moderate supraglottic edema persisted. Movement of the left vocal cord was noted on day 9 after surgery and the tracheostomy was removed 2 wk after surgery.

	Discussion

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Airway obstruction after CEA is well described and can occur from several causes (4). Although the edema seen on FOB assessment was moderate in severity, this was not severe enough to cause respiratory obstruction. Airway edema after CEA is common and may result from tissue edema resulting from surgical trauma, presence of neck hematoma, or interference with venous and lymphatic drainage (5).

Damage to the vagus nerve or recurrent laryngeal nerve may lead to transient or permanent vocal cord paralysis. We postulate that the right recurrent laryngeal nerve was previously damaged during the previous thyroidectomy, leading to paralysis of the right vocal cord. As long as the left vocal cord was functional, the patient remained asymptomatic. However, when the left vocal cord was paralyzed the patient presented with the clinical picture of acute bilateral vocal cord adduction and acute stridor. Thyroid surgery may lead to permanent and transient palsy of the vocal cords in 1% and 2% of patients, respectively (6). This has important implications when subsequent head and neck surgery, such as CEA, is required.

The incidence of unilateral vocal cord paralysis after CEA is reported at between 6% and 4% (7,8). Unilateral vocal cord paralysis may be asymptomatic or present with hoarseness but usually recovers within 12 months after surgery (8). The exact mechanism of vocal cord paralysis remains conjectural. AbuRahma and Lim (9) suggested that nerve injury could occur as a result of excessive manipulation of the carotid sheath or traction injury on the vagus or recurrent laryngeal nerves within the tracheo-esophageal groove. Because the current case was performed in an awake patient, it clearly demonstrates the exact point at which nerve injury occurred. Although there was some stimulation of the nerve during initial blunt dissection and retraction about the carotid sheath, it was when the retractor blade was replaced deep in the wound in proximity of the tracheo-esophageal groove that acute respiratory obstruction occurred.

Prior knowledge of a unilateral vocal cord paralysis has both anesthetic and surgical implications and routine preoperative assessment by indirect laryngoscopy has been recommended when the potential for this condition exists (10). This becomes essential with a history of neck surgery, such as previous contralateral CEA or thyroid surgery. Although not illustrated in this case, cervical plexus block itself may lead to vocal cord paralysis by blocking the vagus or recurrent laryngeal nerve, which course close to the site of injection. This would be of a transitory nature, corresponding to the duration of the local anesthetic. The presence of a preexisting unilateral vocal cord paralysis may contraindicate cervical plexus block because it could lead to the onset of temporary respiratory obstruction if the contralateral vocal cord is affected by the block. The surgical implications include a consideration of carotid stenting as an alternative to open surgery. If open surgery is performed, particular care must be give to any maneuver that may impinge on the vagus or recurrent laryngeal nerve.

	Footnotes

 
Accepted for publication September 7, 2005.

	References

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6. Rosato L, Avenia N, Bernante P, et al. Complications of thyroid surgery: analysis of a multicentric study on 14,934 patients operated on in Italy over 5 years. World J Surg 2004;28:271–6.[Medline]
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