|Year : 2013 | Volume
| Issue : 3 | Page : 306-308
Aphonia following tracheal intubation: An unanticipated post-operative complication
S Vyshnavi, Nalini Kotekar
Department of Anesthesiology, JSS Medical College, Mysore, Karnataka, India
|Date of Web Publication||25-Jul-2013|
Department of Anesthesiology, JSS Medical College and Hospital, MG Road, Mysore - 570 004, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Vyshnavi S, Kotekar N. Aphonia following tracheal intubation: An unanticipated post-operative complication. Indian J Anaesth 2013;57:306-8
|How to cite this URL:|
Vyshnavi S, Kotekar N. Aphonia following tracheal intubation: An unanticipated post-operative complication. Indian J Anaesth [serial online] 2013 [cited 2020 Jan 22];57:306-8. Available from: http://www.ijaweb.org/text.asp?2013/57/3/306/115578
| Introduction|| |
Tracheal intubation is a routine procedure performed by anaesthesiologists. Complications following this procedure are not uncommon and include sore throat, hoarseness of voice, dysphagia, etc. They are minor and resolve spontaneously or with minimal intervention. However, aphonia secondary to vocal cord paralysis following tracheal intubation is a rare complication during routine surgeries, more commonly encountered after thyroid surgeries. , Though not fully understood, certain risk factors have been proposed to explain this phenomenon such as advanced age, comorbid conditions, use of nitrous oxide, patient positioning and difficult intubation. With certain simple measures such as use of appropriately sized endotracheal tube (ETT), monitoring cuff pressure intra-operatively and diligent patient positioning, the occurrence of this complication can be minimized. We report three cases of aphonia secondary to vocal cord involvement, following tracheal intubation, encountered over a period of 12 years in our institute.
| Case Reports|| |
A 32-year-old male patient with Mallampati (MP) I airway was posted for elective laparotomy for excision of hepatic flexure mass. Patient was intubated with 8.5 mm internal diameter (ID) ETT in first attempt. Hoarseness of voice was noted 3 h after extubation and indirect laryngoscopy (IDL) revealed right vocal cord palsy. There was spontaneous resolution of the condition in 40 days.
A 38-year-old male patient with MP II airway was posted for surgery with multiple fractures of right upper limb and soft-tissue injuries on the scalp and face. Patient was intubated with 9 mm ID ETT in first attempt. Patient could not phonate after extubation and IDL revealed wavy distortion of both vocal cords. Patient regained normal voice over 60 days.
A 42-year-old obese female patient with MP III and short neck received general anaesthesia for incisional hernia repair and was intubated with 7 mm ID ETT after three attempts. She had a sore throat in the post-operative period and on the third day, developed loss of voice. IDL revealed slight bowing of left vocal cord and she regained normal voice over 26 days.
There was no history indicative of pre-existing pathology including hormonal disorders (thyroid, parathyroid), metabolic (diabetes mellitus and autonomic neuropathy) or arthritic disorders in any of the patients. Portex® ETTs were used in all patients and cuff was inflated with air and cuff pressure was not monitored.
| Discussion|| |
Post-operative aphonia can be attributed to causes in the region of surgery as in the head and neck, laryngeal or open heart surgeries where injury to recurrent laryngeal nerve is likely to precipitate vocal cord dysfunction. However, aphonia in surgeries of distant region have also been reported, where tracheal intubation itself may have been the culprit. 
Tracheal intubation is associated with several complications such as direct injury to the tissues in the path of intubation, haematomas and avulsion of the vocal cords and arytenoid dislocation.  Vocal cord palsy is a rare and serious complication of tracheal intubation, poorly understood and often alarming for the patient and the anaesthesiologist alike, and with profound legal implications.  The exact mechanism of vocal cord palsy is still not clear. Based on cadaveric studies, Ellis and Pallister proposed injury to anterior branch of recurrent laryngeal nerve as it traverses between the lamina of thyroid cartilage and laryngeal mucosa as a possible mechanism.  The overinflated cuff of ETT can compress the nerve at this location leading to paralysis. Cuff position in trachea too is a critical factor. Pressure neuropraxia can result when the cuff is placed at or just below, the level of vocal cords or if the cuff is not deflated before extubation. It is found that the area 6-10 mm below the vocal cords is most susceptible to injury. Hence, it is recommended that the cuff be placed at least 15 mm below the cords.  Large cuffs have a greater contact area with the laryngeal mucosa and hence, despite lower cuff pressure, result in the greater area of mucosal trauma. Further, pressure inside the cuff does not remain static throughout surgery and is influenced by factors such as diffusion of nitrous oxide or oxygen into the cuff, movement of the head away from the neutral position, coughing and straining on the tube due to light planes of anaesthesia.  Hence, frequent monitoring of cuff pressure intra operatively may be useful in preventing this complication. Instilling the cuff with preservative free lignocaine 4% has been shown to decrease the incidence of hoarseness and post-operative sore throat. Lignocaine tends to diffuse across the cuff and provide local anaesthetic action and attenuate the cough reflex during extubation.  It also helps to maintain a stable intracuff pressure based on the physical principle that liquids do not expand when highly soluble gases dissolve in them. 
Hyperextension of the neck, causing stretching of vagus nerve, which is anchored by the recurrent nerve in the mediastinum has also been implicated.  Other uncommon causes include a concomitant respiratory infection, toxic neuritis, presence of nasogastric tube, infectious neuritis, previously existing asymptomatic palsy and chemical causes (insufficiently aerated ethylene oxide sterilised tubes). ,
Proposed risk factors for vocal cord paralysis are age more than 50 years, prolonged intubation, co-existing diseases such as diabetes and hypertension, smokers, and gastro-oesophageal reflux disease.  Laryngeal tissues degenerate with age and become more susceptible to acute inflammation and microcirculatory insufficiency due to cuff pressure and mechanical damage by the tracheal tube.
The causal relationship between prolonged intubation and vocal cord paralysis is unclear. The tube can cause acute inflammation, erythema, ulceration and granuloma formation, which may induce cord immobility. Increased cuff pressure can injure the recurrent laryngeal nerve causing degeneration and paralysis as also ischemic neuronal degeneration by compromising microcirculation.  Diabetes is associated with peripheral neuropathy, so the nerve may already be functionally abnormal at the time of intubation, and this may worsen thereafter resulting in cord dysfunction. 
Hypertension is associated with atherosclerotic changes in laryngeal vasculature. Hence, compression by the cuff can result in microcirculatory insufficiency in the nerve. 
Differential diagnosis of vocal cord palsy occurring after an intubation include arytenoid dislocation, hereditary neuropathies, synechia of processus vocalis and psychogenic paresis. 
In our first case, increase in cuff pressure due to diffusion of nitrous oxide might have caused compression injury to recurrent laryngeal nerve as also the inadvertent positioning of the tube in the vulnerable area just below the cords. Literature suggests a time period of 6 weeks to 1 year for complete recovery of vocal cord palsy.  However, this patient showed rapid recovery probably because of younger age and no added risk factors. In case 2, the probable cause could have been the repeated movement of the head intra-operatively for better surgical exposure of the injured area resulting in stretching of vagus nerve. Larger cuff of 9.0 mm ID tube used in this case could have contributed to additional local mucosal injury. In case 3, multiple attempts at intubation might have resulted in an acute inflammation of the cords, with additional insult possibly from the pressurised cuff causing degeneration of the nerve.
| Conclusion|| |
Vocal cord paralysis is a rare complication following tracheal intubation, which is difficult to anticipate, but can be prevented with simple measures. It is advisable to individualize the ETT size. The cuff should be positioned at least 15 mm below vocal cords and cuff pressure should be monitored. It is also advisable to inflate the cuff with preservative free lignocaine. Excessive rotation and stretching of the neck should be avoided. Routine implementation of these simple measures in all intubated patients can reduce the incidence of this alarming complication.
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