J Shoulder Elbow Surg (2013) 22, e1-e3
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CASE REPORTS
Isolated contralateral glossopharyngeal and vagal nerve palsy after arthroscopic rotator cuff surgery: a case report Ian King, MRCS Eda,*, Yusef Michla, FRCS (Orth)a, Sanjay Varma, FRCAb, Stephen Aldridge, FRCS (Orth)a a b
Department of Trauma and Orthopaedics, Sunderland Royal Hospital, Sunderland, Tyne & Wear, UK Department of Anaesthetics, Sunderland Royal Hospital, Sunderland, Tyne & Wear, UK
Isolated glossopharyngeal and vagal nerve palsy is a rarely reported phenomenon. We present a patient with unilateral isolated cranial nerve IX and X palsy after arthroscopic rotator cuff surgery on the contralateral shoulder. To our knowledge, this is the first time that this combination of neural injuries has been reported after arthroscopic shoulder surgery, and indeed, the first time that a glossopharyngeal and vagal nerve injury have been described together after an orthopedic operation.
Case report A 65-year-old right hand–dominant shop owner presented with a painful right shoulder. Clinically, there was a painful arc of movement, and reduced power was found in the rotator cuff. Radiographs demonstrated degenerative changes in the acromioclavicular joint and narrowing of the subacromial space, with sclerosis of the greater tuberosity and acromion. A diagnosis of subacromial impingement with possible cuff tear was made. With no improvement seen with physiotherapy, the patient was listed for a right shoulder arthroscopy, rotator cuff repair, and subacromial decompression, which included long head of biceps tenotomy for tendinopathy found at operation. The patient’s medical history included gallstones, psoriasis, hypertension, and most significantly, bilateral cervical sympathectomies for hyperhidrosis in her hands. These were both performed 8 years previously using transthoracic endoscopic Ethics approval was not required for this case report. *Reprint requests: Ian King, Department of Trauma and Orthopaedics, Sunderland Royal Hospital, Kayll Rd, Sunderland, Tyne & Wear, SR4 7TP, UK. E-mail address:
[email protected] (I. King).
approaches to destroy the second thoracic ganglions on each side. The only residual effect was of a bilateral Horner syndrome, which was more prominent on the right side. No neurologic deficit was noted preoperatively. The patient underwent general anesthesia with no regional nerve blocks. The patient was placed in a standard beach chair position with her head held in neutral. The head position was monitored during the patient’s ascent from supine to the beach chair sitting position. At no point was her head turned, and care was taken so the cervical spine was not rotated at all or particularly flexed or extended during positioning. The head position was checked by the surgeon and the anesthetist and was not moved intraoperatively. No central venous access was required. Our routine involves the use of a specific shoulder table with a cut-out behind the shoulder to be operated on and a head restraint that helps to hold the head. The patient’s head was fixed in the padded head restraint, which is part of the table, and further stability was gained by using sleek tape as a forehead and chin strap. The airway, graded Mallampati II, was protected by a 7-mm endotracheal tube for the duration of the 100-minute procedure. No regional anaesthesia was required. The arm was prepared, along with the hand, and allowed to hang free, according to routine. No extensions, such as Spiders, were used to position and hold the limb; however, the arm would occasionally encounter mild traction from an assistant for short periods when the subacromial space was inspected intraoperatively. The shoulder operation proceeded without event, requiring standard posterior and anterosuperior ports and additional lateral and anterolateral portals for further visualization and working. The patient’s physiologic parameters were stable throughout the operation, with the target arterial pressure of 90 mm Hg well maintained to minimize articular bleeding. Extubation was unremarkable, and the patient was moved to the recovery room. The patient experienced swallowing difficulties postoperatively, specifically, nasal regurgitation in the absence of
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e2 dysphagia. There was no airway compromise, sore throat, or voice change. A normal result on a comprehensive neurologic examination, with no visual or sensory disturbance or focal limb or other cranial nerve abnormalities, suggested a perioperative stroke was unlikely. An ear, nose, and throat examination demonstrated a left palatal weakness and a less mobile left vocal cord, although full glottis closure could be achieved and the gag reflex was preserved. A speech and language assessment with videofluoroscopic studies showed evidence of incoordination in the upper pharynx and reduced left pharyngeal squeeze in the presence of normal lip and tongue movements and good velar closure. An endoscopic swallowing assessment showed premature spillage of liquids and reduced left pharyngeal squeeze but no aspiration. Magnetic resonance imaging (MRI) of the head and neck was unable to identify any anatomical abnormality. The diagnosis was of a left glossopharyngeal and partial vagus nerve palsy manifesting in an incomplete left palatal palsy and a left vocal cord palsy. The patient underwent regular review, and after 3 months, the symptoms had resolved. Postoperatively, the shoulder regained a full, pain-free range of movement, with no functional deficit.
Discussion Injury to cranial nerves after arthroscopic surgery is a very rarely reported complication.1,6 There is little in the literature about isolated glossopharyngeal and vagal palsies, and nothing documented to date in association with an orthopedic operation. Shoulder surgeons over the years have come to appreciate the importance of patient position in arthroscopy, not only for operative ease but also with respect to risk of neural injuries, mostly of the brachial plexus or nerves of forearm from traction and anatomic distortion.11 Arthroscopic procedures that require extension of the neck potentially increase the risk of neural damage. The beach chair position has been widely advocated as an alternative to the lateral decubitus position, which has been seen to be associated with such injuries.9,15 To facilitate patient positioning and alignment for such procedures, there now exist a number of specially designed operating theater tables for shoulder surgery. The glossopharyngeal nerve, exiting the upper medulla rostral to the vagus nerve, emerges from the jugular foramen on the lateral side of the inferior petrosal sinus. At the jugular fossa, the tympanic branch leaves the nerve and enters the temporal bone, ultimately supplying a sensory component to the bony part of the auditory tube, middle ear, and mastoid air cells, and via the lesser petrosal nerve, a parasympathetic supply to the parotid and other salivary glands. The glossopharyngeal nerve continues down between the internal jugular vein and the internal carotid artery, swinging anteriorly over the artery, beneath the styloid process around to the lateral side of stylopharyngeus, where it gives off its motor branch to that muscle and contributions to the pharyngeal plexus. Descending from the surface of the middle pharyngeal constrictor, it passes deep to the hyoglossus muscle and is then distributed to the tongue and oral mucous glands.14
I. King et al. The vagus nerve leaves the medulla between the medullary pyramid and the inferior cerebellar peduncle to emerge through the jugular foramen. The nerve descends straight down the neck in the carotid sheath, in between and posterior to the carotid artery and jugular vein, entering the mediastinum anterior to the subclavian artery. Of the intermediate branches, the pharyngeal branch passes anteriorly between internal and external carotid arteries to join the pharyngeal plexus on the middle constrictor, supplying the pharynx (except stylopharyngeus) and the soft palate (except tensor veli palatini). The course of the recurrent laryngeal nerve is well-described, differing on both sides to supply the trachea, esophagus, part of the inferior constructor, and all laryngeal muscles, except for the cricothyroid, which is innervated by the external branch of the superior laryngeal nerve.14 Injury to the hypoglossal nerve has been reported in association with arthroscopic shoulder surgery using endotracheal ventilation,1,6,12 but no cause was found. A literature search illustrates that endotracheal intubation can be associated with neuropraxia of the hypoglossal nerve,18 but damage to the glossopharyngeal nerve has not been recorded. Hypoglossal nerve palsies have been previously described with the use of laryngeal mask airways, but again, these are rare and can be unilateral7,13 or bilateral.17 In both laryngeal and endotracheal approaches, head and neck position and cuff pressures and size are postulated as factors to have played a part in a palsy developing. Damage to nerves from intubation has been noted elsewhere10 and could explain part of the presentation. A study examining neural injuries in thyroid surgery demonstrated that 3 patients in a cohort of 210 (1.4%) sustained intubationrelated recurrent laryngeal nerve palsies.4 No comment was made describing a simultaneous palatal palsy in these patients; however, recurrent laryngeal nerve palsy alone failed to explain our patient’s symptoms. Transient cranial nerve palsies have been seen in other surgical procedures, such as after open heart surgery,16 although causation is often difficult to ascertain. Glossopharyngeal nerve palsies, in particular, have been seen with carotid dissections, glossopharyngeal schwannomas, and extracranial internal carotid artery aneurysms.20 Acquired asymmetrical palatal palsies were described in three children, with symptoms including abnormalities of the palatal components of speech and nasal escape of fluids, with MRIs that appeared normal, that were believed to be secondary to a viral infection.3 Unfortunately, no organisms were identified to support this hypothesis, but all patients made a complete and spontaneous recovery to normal over a few weeks. Glossopharyngeal and vagal nerve palsies have been observed together previously, although such cases are mostly secondary to central pathology, such as syringomyelia with syringobulbia5 presenting with isolated cranial nerve IX and X paralysis, cranial fractures, infection with herpes zoster, or due to transient ischemic events.19 Walther and Alevisopoulos19 described a patient presenting with dysphagia and
Case: glossopharyngeal and vagus nerve palsy aspiration. Examination showed a Horner syndrome and paralysis of the soft palate and one vocal cord, with asynergic swallow on videofluoroscopy. Brainstem MRI showed enhancement in the upper medulla oblongata, which later was seen to resolve in correlation with the patient’s symptoms. Our patient underwent a vigorous examination, and the MRI appeared entirely normal. In a patient with a history of previous neck surgery, the existence of preoperative Horner syndrome makes interpretation of the pathologic picture all the more difficult. Caparros-Lefebvre et al2 hypothesized that cranial nerves IX, X, and XII might be at risk of a cranial nerve ischemic arterial syndrome to explain such unilateral palsies with normal imaging. Their patient presented after a generalized seizure. Cranial nerve XI is spared, in contrast to IX, X, and XII, because this has a double vascular supply that provides collateral flow in occlusions. A plausible explanation for our patient’s symptoms could be found in a condition known as Avellis syndrome, or palatolaryngeal hemiplegia. This neurologic disorder results from vertebral artery occlusion leading to lesions of the nucleus ambiguous and pyramidal tract and involves vocal cord and soft palate paralysis on one side, with contralateral loss of temperature and pain sensation. Although originally described involving the vagus and glossopharyngeal nerves, anatomically related cranial nerves have also been observed to be involved. This has been reported in association with trauma8 but not in association with orthopedic interventions. For our patient, the accessory nerve was fully functioning, which further stood against such an explanation. In addition, testing of temperature sense was not documented, which makes this diagnosis impossible to make, particularly once the symptoms have resolved.
Conclusion With the patient’s head in an upright position, and with the use of muscular relaxants, the patient’s head is potentially susceptible to positional change and misplacement. We accordingly postulate that the use of endotracheal intubation or head position may have resulted in this neural damage, although the pattern of the injury is unusual in this respect and does not easily align with previously described cases. We therefore recommend vigilance, not only in the maintenance of head and neck position when patients are in the beach chair position but also of patients as they recover to ensure that no undue complications go unnoticed and therefore untreated.
Disclaimer The authors, their immediate families, and any research foundations with which they are affiliated have not
e3 received any financial payments or other benefits from any commercial entity related to the subject of this article.
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