Abstract

Perioperative hypoglossal nerve palsy is a rare postoperative complication. Here, we present a case of transient unilateral hypoglossal nerve palsy after shoulder surgery. The cause of the hypoglossal nerve palsy in our patient was assumed to be a complication of oropharyngeal manipulation during orotracheal intubation for general anesthesia. However, direct compression of the hypoglossal nerve beneath the angle of the mandible during mask ventilation and the surgical procedure may have been a concomitant cause. Therefore, in order to prevent this complication, we must perform mask ventilation and direct laryngoscopy carefully. Head and neck manipulation should be gentle during anesthesia for shoulder surgery.

Keywords

arthroscopy; hypoglossal nerve diseases; palsy; postoperative complications; posture; shoulder joint;

1. Introduction

General anesthesia (GA)-related complications in shoulder surgery have appeared in numerous reports as anecdotes and include fatal air embolism, tracheal compression, temporary blindness, pneumothorax, quadriplegia, complete airway obstruction secondary to extravasation of fluid into the mediastinum, potentially fatal epinephrine-induced arrhythmia, negative pressure pulmonary edema, pneumomediastinum, injury to the sciatic, peroneal and brachial plexus nerves, obstruction of the internal jugular vein, postural hypotension and cerebral ischemia.^1,2 Here, we report a case of transient unilateral hypoglossal nerve palsy following shoulder surgery under GA. We review the literature and discuss the etiology.

2. Case Report

A 57-year-old man had progressive pain and disability in both shoulders for about 1 year. A rotator cuff tear was diagnosed by magnetic resonance imaging. The symptoms did not improve despite medical therapy and rehabilitation. Arthroscopy was advised. There were no significant events in his past medical history and he had not received any surgery. Previous laboratory examinations revealed nothing remarkable.

GA was induced with intravenous propofol and fentanyl, and muscle paralysis was obtained with cisatracurium. A size 7.5-mm endotracheal tube (ETT) was gently placed with a Macintosh blade. No difficulty in laryngoscopy and intubation was encountered. The cuff of the tube was inflated to a cuff pressure of less than 20 cmH₂O. The ETT was secured at the right mouth angle. The patient was placed in a semi-beach-chair position with the knees in flexion. The head and neck were secured in the neutral position with two straps. Arthroscopy was done to expose the left rotator cuff and acromion process. Fibrosis and tendonitis had affected the bursa and the rotator cuff following repeated episodes of mechanical inflammation. There was osteophyte formation over the acromion process, and degenerative traction spurs developed in the coracoacromial ligament. The tear of the rotator cuff was repaired with sutures. The operation lasted for 108 minutes. Anesthesia was maintained with target-controlled infusion of propofol and titrated intravenous fentanyl and cisatracurium. The patient was awakened and extubated in the operating room without difficulty.

Two hours later, he complained of difficulty in swallowing and his speech was slurred. Numbness and paralysis of the left side of the tongue were found. Neurological examination revealed that the tongue deviated toward the left, but the uvular and vocal cords were undamaged (Figure 1). The results of computed axial tomography and magnetic resonance imaging of the brain were normal without ischemia, tumor, or hemorrhage. The results of neck Doppler excluded the possibility of dissection of the internal or external carotid artery. The neurologist and otolaryngologist jointly made the diagnosis of isolated left hypoglossal nerve palsy based on the findings of preceding studies. Tongue mobility gradually improved within 3 days and the symptoms partially resolved after acupressure and rehabilitation. The patient’s symptoms resolved completely 3 weeks later.

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Figure 1 Tongue deviates toward the left side on pro- trusion on postoperative day 3.

3. Discussion

From the data reported in the literature, as with our case, complete recovery of function from hypoglossal nerve palsy is generally achieved within the first 6 months. This progressive but slow recovery of function suggests that the nerve damage is of a neuropraxic type, typical of compression injury.³

The incidence of perioperative isolated hypoglossal nerve palsy is very low.⁴⁻⁷ Dziewas and Ludemann³ recorded 27 cases of hypoglossal nerve palsy after surgery, of whom 25 and two cases sustained the complication after intubation GA and laryngeal mask airway GA, respectively. Of the 25 cases, only five were subjected to left hypoglossal nerve palsy after intubation GA,^6,8−12 as occurred in our case. Paralysis of the hypoglossal nerve is a multietiological condition. One of the etiologies associated with anesthesia was oropharyngeal manipulation such as stretch of the nerve against the greater horn of the hyoid bone by a laryngeal mask or orotracheal tube or compression of the nerve by the posterior part of the laryngoscope or orotracheal tube, distension of the nerve during intubation with cricoid pressure, and inadvertent extubation of the tracheal tube with its cuff remaining inflated.^8,11−14 Prolonged use of a gag with an excessively long blade to manipulate the lateral tongue base and expose the lower poles during tonsillectomy7 may reinforce the nerve damage. Otherwise, direct compression of the hypoglossal nerve beneath the angle of the mandible,⁹ internal carotid artery dissection,¹⁵⁻¹⁷ and central venous catheterization via the internal jugular vein^18,19 may be the possible etiologies of postoperative hypoglossal nerve palsy. According to the aforementioned etiologies, we speculate that the mishap in our case might have occurred because of direct stretch of the nerve against the greater horn of the hyoid bone by ETT, or compression of the nerve by the posterior part of the laryngoscope or ETT. However, we had another possibility in mind that direct compression of the nerve beneath the angle of the mandible by fingers during mask ventilation might be the cause of the injury.

In addition, we agree with Mullins et al,⁹ who reported a similar case and postulated that a change in the position of the neck at some points caused the nerve to be compressed beneath the angle of the mandible. This may have occurred at any time, although it seems most likely that it happened when the back support was lowered from an angle of 70º to the floor to one of 30º, before the surgical procedure was performed. The hypoglossal nerve (the 12^th cranial nerve) originates from the hypoglossal nucleus of the medulla oblongata between the olive and pyramid and leaves the skull through the hypoglossal canal. It then descends between the internal carotid artery and internal jugular vein and passes inferiorly to the angle of the mandible. Therefore, the strap used to secure the head in the natural position might compress the nerve. Moreover, we found that the first surgical assistant’s elbow was very likely to compress the mandible angle during surgery. We currently recommend that, when the beach-chair position is used, the position of the patient’s head and the assistant surgeon’s elbow should be watched closely, not only by the anesthesiologist but also by the chief surgeon and nursing staff.

Although hypoglossal nerve palsy after intubation, bronchoscopy or use of a laryngeal mask airway appears to be exceptionally rare, this complication should be known to anesthesiologists and neurologists, because they will be consulted for the correct diagnosis, etiology, and prognosis with respect to therapeutic measures. A differential diagnosis to distinguish hypoglossal nerve, lingual nerve, and recurrent laryngeal nerve problems is necessary and is largely dependent on the clinical manifestation since these nerve injuries may be concomitant. Lingual nerve injury usually presents as loss of taste and sensation of the anterior tongue. Hypoglossal nerve injury causes difficulty in swallowing. Recurrent laryngeal nerve injury manifests as dysarthria, stridor or postoperative aspiration. Computed axial tomography and magnetic resonance imaging of the brain could provide information for exclusion of a cerebrovascular accident or a mass lesion. Otherwise Doppler examination of the neck should be done to exclude the possibility of internal or external carotid artery dissection. Finally, rehabilitative measures which may include dietary modifications and logopedic training are recommended.³

In conclusion, the cause of hypoglossal nerve palsy in our patient was assumed to be a complication of direct compression of the hypoglossal nerve beneath the angle of the mandible during the surgical procedure with mask ventilation and oropharyngeal manipulation. Therefore, in order to prevent this complication, we must apply mask ventilation and direct laryngoscopy delicately and carefully by gently manipulating the patient’s head and neck, and by paying attention to the strap used to secure the patient’s head and neck and to compression of the nerve by the surgeon’s elbow during surgery.