Management of bilateral recurrent laryngeal nerve paresis after thyroidectomy.

Bilateral recurrent laryngeal nerve (RLN) injury is rare for benign thyroid lesions (0.2%). After extubation-stridor, respiratory distress, aphonia occurs due to the closure of the glottic aperture necessitating immediate intervention and emergency intubation or tracheostomy. Intra-operative identification and preservation of the RLN minimizes the risk of injury. It is customary to expect RLN problems after thyroid surgery especially if malignancy, big thyroid, distorted anatomical problems and difficult airway that can lead to intubation trauma. Soon after extubating, it is essential to the anesthetist to check the vocal cord movements on phonation and oropharyngeal reflexes competency. But this case is specially mentioned to convey the message that in spite of absence of above mentioned predisposing factors for complications and good recovery profile specific to thyroid, there can be unanticipated airway compromise that if not attended to immediately may cost patient's life. This is a case of postextubation stridor following subtotal thyroidectomy due to bilateral RLN damage and its management.

INTRODUCTION

Bilateral recurrent laryngeal nerve (RLN) injury following surgery for benign thyroid lesion is rare. Preoperative indirect laryngoscopy is very essential. Intra-operative identification of the nerve along its tract and preservation minimizes the risk of injury. Intra-operative continuous RLN monitoring may be useful in certain cases, but it is time-consuming, requires spontaneous ventilation and increased incidence of false negatives. Controlled trials have shown no statistical reduction in paralysis, paresis, or total injury rates to the RLN with RLN monitoring.[1] Intensive postoperative clinical monitoring is essential even though there is a good recovery profile, apparently normal vocal cord movements on inspection and positive cuff leak test after thyroid surgeries. Careful postoperative vigilance and timely response can mitigate life-threatening complications.

CASE REPORT

A 45-year-old, 50 kg female with multinodular goiter was posted for subtotal thyroidectomy. The preanesthetic assessment revealed no significant abnormality and patient was in the euthyroid state (T3-1.26 ng/dl, T4-8.21 mcg/dl, thyroid-stimulating hormone - 4.0 mIU/ml). Antero posterior and lateral radiographs of the neck showed no evidence of compression of the trachea. Patient was referred to Department of Otolaryngology for indirect laryngoscopy prior to surgery; that revealed normal appearance and movements of vocal cords.

The patient was scheduled for surgery. Nil per oral status was maintained, and 0.25 mg tablet alprazolam was given the night before surgery. General anesthesia was administered with 50 mg of injection ranitidine, 4 mg of injection ondansetron, 1 mg of injection midazolam, 0.2 mg of injection glycopyrrolate intravenously as premedications after attaching the monitors in the preoperative room. Patient was shifted to the operation room. Induction was done with 250 mg of injection thiopentone sodium intravenously, and relaxation was facilitated with 5 mg of injection vecuronium after preoxygenating with 100% oxygen for 3 min. A 7½ mm ID cuffed reinforced endotracheal (ET) tube was inserted after gentle laryngoscopy. Maintenance was done with vecuronium, N2O:O2 = 5:3 and sevoflurane (0.25–0.5%). A 100 mcg of injection fentanyl was given for intra-operative analgesia. Subtotal thyroidectomy was performed and intra-operative period was uneventful with minimal blood loss. At the end of the procedure, the patient was reversed; cuff leak test was positive indicating no evidence of tracheomalacia and was extubated successfully. Postextubation, direct laryngoscopy revealed the cords movements and appearances were normal. After ensuring thorough recovery and good vocalizing, patient was shifted to postoperative room.

After an hour in the recovery room, patient had an inspiratory stridor with signs of respiratory distress (tachypnea, tachycardia, flaring of alar nasae, restlessness) and there was a gradual fall in the saturation to high 80's to low 90's. There was no local swelling at the surgical site. We tried to ventilate with a FiO2 of 100%, and Larson's jaw thrust was applied, but saturation did not improve much. After sedation, as vocal cords were in adduction on laryngoscopy, patient was intubated with a smaller size (7 mm ID) cuffed ET tube using bougie and connected to a T-piece. Patient could maintain stable vitals after the procedure. Bilateral RLN paresis was confirmed with flexible fiber optic laryngoscopy by otolaryngologist (after trial extubation), and tracheostomy [Figure 1] was performed to prevent further respiratory complications and facilitate early mobilization [Figure 2]. Patient was de-cannulated 14 days later with the return of adequate cord function.

Figure 1

Tracheostomy being performed

Figure 2

Patient after tracheostomy

DISCUSSION

The innervations of larynx are:

Superior laryngeal nerve gives sensory supply to the supraglottic mucosa, and external branch gives motor supply to the cricothyroid muscle

RLN gives motor supply to intrinsic laryngeal muscles (abductors) and sensory supply to mucosa below vocal cords.

Incidence of respiratory complications at extubation and in the recovery room is greater than at intubation that are as follows:[234]

Hematoma (0.79–1.2%)

Laryngeal edema (0.19%)

Hypoparathyroidism, temporary: 0.9–8.3%, permanent: <1.7%

Stridor

Hypocalcemia

Dysphagia (1.4%)

Bilateral RLN palsy (0.4–1.9%) and bilateral RLN paresis (0.2%) in thyroidectomies for benign lesions[5]

Infection (0.3%)

Tracheomalacia.

Injury to the RLN can occur by a number of mechanisms such as ischemia, irritation of the nerve without actual damage,[5] contusion, entrapment, and actual transection.[6] Higher risk of damage occurs in malignancy and secondary operations.[6] Anatomic variability and distortions will increase the risk of nerve injury.[6] This can be prevented by:[6]

Preoperative laryngoscopy: 1.9% of patients without and 3% of patients presenting with carcinoma of the thyroid have unilateral/ipsilateral RLN palsy preoperatively

Complete dissection and exploration of RLN during surgery

Visualization required along the distance between branching of inferior thyroid artery and entry of nerve into the cricothyroid cartilage

Awareness of anatomical variations.

Continuous RLN monitoring may be useful in certain cases; but is time-consuming, requires spontaneous ventilation and increased incidence of false negatives. Controlled trials of continuous RLN monitoring have shown no statistical reduction in paralysis, paresis, or total injury rates to the RLN.[1] Deep extubation can be performed with spontaneous breathing to observe vocal cord movement.[17] If there is partial injury, recovery is seen in weeks. The various therapeutic strategies for managing bilateral RLN palsies are reintubation (if paralyzed in para-median position) and tracheostomy.[689] Other surgical options are endoscopic posterior ventriculocordectomy, nerve decompression from ligatures or scar tissue, glottic widening procedures after 6 to 9 months.[10]

CONCLUSION

Careful postoperative observation is very essential in patients undergoing thyroidectomy, as life threatening complications like RLN palsies if unnoticed can occur in seemingly normal patients.