Post Thyroidectomy Bilateral Recurrent Laryngeal Nerve Palsy – Not Always Surgical!

Case Report

Annals Thyroid Res. 2017; 3(1): 87-88.

Post Thyroidectomy Bilateral Recurrent Laryngeal Nerve Palsy – Not Always Surgical!

Rajaram Burrah¹*, K Shivakumar¹, Vidya Bhushan² and Balasubramanyam AM²

¹Department of Surgical Oncology, St. John’s Medical College Hospital, India

²Department of Otorhinolaryngology, St. John’s Medical College Hospital, India

*Corresponding author: Rajaram Burrah, Department of Surgical Oncology, St. John’s Medical College & Hospital, Sarjapur Road, Bangalore, Karnataka, India

Received: November 02, 2016; Accepted: January 16, 2017; Published: January 23, 2017


Importance: The cause of Recurrent Laryngeal Nerve (RLN) palsy following thyroidectomy is usually attributed to the surgery. Rarely, however, the cause can be non-surgical and results in adductor palsy. The management of these patients is different and is prudent that surgeons be aware of this entity.

Observation: We encountered a patient who developed bilateral RLN palsy following total thyroidectomy. The clinical finding and recovery were suggestive of a non-surgical cause for the palsy. We reviewed the literature and also performed a cadaver dissection to better understand the anatomy of RLN and cause of the palsy.

Conclusion: The non-surgical cause of RLN palsy (adductor palsy) presents differently from that of the surgical cause. The presentation and treatment are also different. Tracheostomy is not required and recovery of the nerve is usually the norm.

Keywords: Recurrent laryngeal nerve; Total thyroidectomy; Palsy


Recurrent Laryngeal Nerve (RLN) palsy occurring following thyroidectomy is a known complication. In most instances it is assumed that the cause of the nerve injury is surgical. However, in spite of meticulous surgery and preservation of the nerves, rarely the cause of RLN palsy could be unrelated to surgery. We encountered one such case where the patient developed bilateral adductor vocal cord palsy following total thyroidectomy. We felt the cause for the palsy is not related to the surgery. We present the events that occurred in our patient and discuss how the management of these patients should be different from those with a surgical cause of RLN palsy.

Case Report

A 32 year old female was referred to our department for the surgical management of her toxic multinodular goiter. The patient gave a history of a neck swelling since 1 year, associated with weight loss and palpitations for 6 months. Following the diagnosis of toxic multinodular goiter she had been started on antithyroid medication. Examination revealed a multinodular goiter involving both lobes measuring 6 x 5 x 4cm. Patient had no voice symptoms and an office laryngoscopy showed bilateral normal mobile vocal cords. Total thyroidectomy under general anesthesia was planned. Patient was induced with Propofol, intubated with a cuffed flexometallic endotracheal tube (size 7mm) and maintained with isoflurane, nitrous oxide and oxygen. During the intraoperative period the entire course of both RLNs was identified and the nerves preserved. No electrocautery was used in the vicinity of the nerves. All the major blood vessels were ligated and divided only after identifying the RLNs. No anatomical variation of the RLNs was noted. Duration of surgery was three hours and twenty minutes, and the patient was positioned in the traditionally described extended position throughout the surgery. General anesthesia was reversed with neostigmine and patient was extubated smoothly. The immediate post operative period was uneventful. Three hours post operatively, the patient was noted to have a breathy voice and developed cough on taking oral feeds. She had no breathing difficulty or stridor. Laryngoscopic evaluation revealed bilateral fixed vocal cords with a wide phonatory gap of around 8 mm (Figure 1). There was no evidence of edema or signs of trauma. The patient was started on naso-gastric tube feeds and was referred to our speech therapist for vocal cord adduction exercises. The histopathological examination of the resected thyroid gland was suggestive of nodular colloid goiter. The patient was started on replacement dose of thyroxine and advised to review after two weeks. After fourteen days, office laryngoscopic examination revealed flickering movements of the vocal cords with a persistent phonatory gap. Though the voice appeared unchanged to us, the patient felt there was an improvement in her voice. She was tolerating soft food orally but had persistence of aspiration to liquid feeds and hence was advised to continue tube feeds. Six weeks post surgery the patient, visibly relieved, came to the clinic with a normal voice and was able to eat and drink normally. Repeat office endoscopy showed bilateral normal and mobile vocal cords with complete adduction (Figure 2). The naso-gastric tube was removed and the patient was advised to follow-up regularly.