We experienced bilateral cranial nerve damage as a rare complication of orotracheal intubation during general anaesthesia for lumbar discectomy. This underlines the importance of head, neck and cervical spine padding in the operative prone position and the meticulous and correct performance of routine manoeuvres of airway management.
Various cases of pressure-associated postoperative dysfunction of the hypoglossal, recurrent laryngeal, external branch of the laryngeal and lingual nerve have been described after the use of laryngeal masks, tracheal tubes and laryngoscopy.1 The combination of unilateral hypoglossal and laryngeal recurrent nerve palsy was first described in 1906 as Tapia's syndrome. In our department, a 52-year-old male patient (178 cm, 80 kg), suffering from a herniated lumbar disc, was scheduled for elective lumbar discectomy. His surgical history included a septal reconstruction with an uvulopalatopharyngoplasty because of obstructive sleep apnoea and a microlaryngoscopy for resection of a single right vocal cord polyp 6 years before. All previous surgeries were uneventful and subsequent tracheal intubations had been performed without any complications. The preoperative neurological and anaesthetic examination was normal (American Society of Anesthesiologists physical status I, Mallampati I). General anaesthesia was induced by intravenous administration of propofol and sufentanil, with neuromuscular blockade obtained with rocuronium. Direct laryngoscopy was performed using a Macintosh blade size 3 (Heine company, Herrsching, Germany). A 7.5-mm tracheal tube was placed without difficulties and was secured at 22 cm in the right mouth angle, once correct placement had been confirmed by positive capnography and auscultation of both lungs. The cuff of the tracheal tube was inflated to a maximal pressure of 30 cmH2O. General anaesthesia was maintained with oxygen (30%), propofol and remifentanil for 70 min. For lumbar discectomy, the patient was placed in the prone position using a thoracolumbar positioning pillow, and the head laid in 20° retroflexion supported by a silicone headrest. During surgery (55 min), no significant changes in cardiovascular or respiratory parameters or neurosurgical abnormalities occurred. Prompt repositioning into the supine position was performed after surgery. The tracheal tube was carefully removed when spontaneous respiration and muscle tone were adequate. Two hours after surgery, the patient complained of a feeling of swelling and hypomotility of the tongue. The airway was clear, with no signs of allergic reaction, dyspnoea or dysphagia, and vital signs were stable. Within 24 h, the patient subsequently developed severe dysarthria and dysphagia. Neurological and ear, nose and throat (ENT) assessment revealed a bilateral hypoglossal palsy with bilateral high-grade palsy of the tongue, a maximal motility of 0.5 cm in all directions and right-sided vocal cord palsy. No pharyngeal cicatrisation was seen. The patient's voice was hoarse and his articulation severely impaired. He had dysphagia with a high risk of aspiration. Computed tomography of the head and neck including angiography as well as cranial MRI were normal. Acute therapy with intravenous administration of high-dose steroids (24 mg dexamethasone/day) was continued for 4 days. Testing of C1-esterase inhibitor levels and activity revealed normal values. Electromyography 7 days postoperatively showed signs of neurapraxia of the vocalis muscle (thyroarythaenoideus) as well as the cricothyroideus and cricoarythaenoideus (posticus) muscle. Within the first 8 weeks, the patient developed distinct symmetric atrophy of the tongue muscles, whereas tongue motility did not improve significantly. Minor activation of the right vocal cord as a sign of laryngeal paralysis was observed by laryngoscopy. Under continuous speech therapy and pharyngeal stimulation, dysarthria and dysphagia improved. The right tongue muscles recovered fully but the patient's left hypoglossal palsy and left tongue hemi-atrophy persisted for 12 months postoperatively and were accompanied by several atrophic spots. Follow-up laryngoscopy showed an almost complete recovery of the laryngeal paralysis. No dysphonia was observed. The patient did not attend the follow-up electromyography assessment for a qualitative evaluation of a possible reinnervation procedure.
A combined bilateral hypoglossal palsy and unilateral laryngeal recurrent nerve palsy with bilateral paralysis of the tongue and unilateral vocal cord paralysis occurred in a patient secondary to lumbar discectomy performed under general anaesthesia. To date, only one case with this combination of damage to three nerves has been described.2 Bilateral hypoglossal nerve palsy is very rare and tracheal tube malposition or increased tracheal tube cuff pressure by laryngoscopy3 or airway management should be considered as possible causative mechanisms for this condition. Two cases of bilateral hypoglossal palsy secondary to tracheal intubation are mentioned in current reports.3,4 Bilateral Tapia's syndrome was described after a rhinoplasty with firm pharyngeal throat packing.5 As the hypoglossal nerve has a superficial course beneath the angle of the mandible, nerve damage is possible during mask ventilation.6 Based on the anatomical course of the hypoglossal nerve along the anterior surface of the transverse process of the first cervical vertebra,7 neck hyperextension in prone position during surgery in combination with the presence of a predisposition for calcification of the stylohyoideum ligament can cause a compression of the nerve against the greater horn of the hyoid bone.7
In summary, the reported bilateral hypoglossal and unilateral right recurrent nerve palsy occurred most likely to a combination of direct nerve pressure through the tracheal tube and stretching of the nerve by neck overextension in prone position. Prevention of this rare complication is based on the recognition of the potential for nerve injury during airway management, tracheal tube cuff inflation and surgical positioning of the patient's head and neck. Attentive knowledge of the anatomical course of the hypoglossal nerve, recurrent laryngeal and vagal nerve are compulsory to prevent this rare but clinically significant complication, as it relates to the positioning of the head and neck and the use of airway instrumentation.
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