Vocal cord paralysis
Vocal cord paralysis: Excerpt from Professional Guide to Diseases (Eighth Edition)
Vocal cord paralysis results from disease of or injury to the superior or, most commonly, the recurrent laryngeal nerve. It may also be congenital.
Causes
Vocal cord paralysis commonly results from the accidental severing of the recurrent laryngeal nerve, or of one of its extralaryngeal branches, during thyroidectomy. Other causes include pressure from a thoracic aortic aneurysm or from an enlarged atrium (in patients with mitral stenosis), bronchial or esophageal carcinoma, hypertrophy of the thyroid gland, trauma (such as neck injuries) and intubation, and neuritis due to infections or metallic poisoning. Vocal cord paralysis can also result from hysteria and, rarely, lesions of the central nervous system.
Signs and symptoms
Unilateral paralysis, the most common form, may cause vocal weakness and hoarseness. Bilateral paralysis typically produces vocal weakness and incapacitating airway obstruction if the cords become paralyzed in the adducted position.
PEDIATRIC TIP Children may present with hoarseness, aspiration, and stridor. If the paralysis is unilateral, it typically involves the left recurrent laryngeal nerve. In unilateral paralysis, airway intervention involving intubation and tracheostomy is rarely indicated; it’s usually required if the paralysis is bilateral.
Diagnosis
The patient history and characteristic features suggest vocal cord paralysis.
CONFIRMING DIAGNOSIS Visualization by indirect laryngoscopy shows one or both cords fixed in an adducted or partially abducted position and confirms the diagnosis.
X-ray or computed tomography scan detect abnormalities in the mediastinum that may be responsible for the injury.
Treatment
Treatment for unilateral vocal cord paralysis consists of injection of Teflon into the paralyzed cord, under direct laryngoscopy. This procedure enlarges the cord and brings it closer to the other cord, which usually strengthens the voice and protects the airway from aspiration. Thyroplasty also serves to reposition the vocal cord, but in this procedure an implant is placed through a neck incision. The ansa cervicalis nerve transfer allows for reinnervation of the muscles of the vocal cord. Bilateral cord paralysis in an adducted position necessitates a tracheostomy.
Alternative treatments for adults include endoscopic arytenoidectomy to open the glottis, and lateral fixation of the arytenoid cartilage through an external neck incision. Excision or fixation of the arytenoid cartilage improves airway patency but produces residual voice impairment.
Treatment for hysterical aphonia may include psychotherapy and hypnosis.
Special considerations
If the patient chooses direct laryngoscopy and Teflon injection, explain these procedures thoroughly. Tell him these measures will improve his voice but won’t restore it to normal. Patients are sometimes placed on voice rest for 24 to 48 hours to reduce stress on the vocal cords, which would increase the edema and might lead to airway obstruction.
Many patients with bilateral cord paralysis prefer to keep a tracheostomy instead of having an arytenoidectomy; voice quality is generally better with a tracheostomy alone than after corrective surgery.
If the patient is scheduled to undergo a tracheostomy:
❑ Explain the procedure thoroughly, and offer reassurance. Because the procedure is performed under a local anesthetic, the patient may be apprehensive.
❑ Teach the patient how to suction, clean, and change the tracheostomy tube.
❑ Reassure the patient that he can still speak by covering the lumen of the tracheostomy tube with his finger or a tracheostomy plug.
If the patient elects to have an arytenoidectomy, explain the procedure thoroughly. Advise the patient that the tracheostomy will remain in place until the edema has subsided and the airway is patent.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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