Airway

REVIEW ARTICLE
Year
: 2019  |  Volume : 2  |  Issue : 2  |  Page : 57--63

Voice loss following endotracheal intubation: The anaesthesiologist's dilemma


Nalini Kotekar, Sriram Vyshnavi 
 Department of Anaesthesia, JSS Academy of Higher Education and Research, Mysore, Karnataka, India

Correspondence Address:
Dr. Sriram Vyshnavi
20, Block 11, Madhuvana Layout, Shrirampura Second Stage, Mysore - 570 034, Karnataka
India

Abstract

Endotracheal intubation is a routine procedure performed by anaesthesiologists worldwide. It is as routine as the placement of a peripheral intravenous catheter. Albeit the gold standard for securing the airway, endotracheal intubation comes with it's share of adverse effects, one of the worst being loss of voice or aphonia. A literature search in major medical databases revealed useful information about the aetiopathogenesis, various mechanisms and risk factors leading to vocal symptoms and acoustic variations. Patient risk factors such as age and co-morbid conditions and anaesthetic considerations such as size of endotracheal tube, number of attempts, mean cuff pressure, anaesthetic agents used and nature and duration of surgery all seem to have a role in this intriguing problem. This review also includes cases we have personally come across in our practice. Based on our experience of cases that we have come across, we propose an algorithm to avoid such a problem.



How to cite this article:
Kotekar N, Vyshnavi S. Voice loss following endotracheal intubation: The anaesthesiologist's dilemma.Airway 2019;2:57-63


How to cite this URL:
Kotekar N, Vyshnavi S. Voice loss following endotracheal intubation: The anaesthesiologist's dilemma. Airway [serial online] 2019 [cited 2019 Dec 11 ];2:57-63
Available from: http://www.arwy.org/text.asp?2019/2/2/57/265619


Full Text



 Introduction



Every year, millions of patients undergo laryngoscopy and tracheal intubation as part of their airway management in the perioperative period. However, intubation is associated with adverse consequences such as hoarseness of voice, sore throat, dysphagia, arytenoid dislocation, oropharyngeal injuries, haematoma, laceration and broken teeth.[1] The incidence of laryngopharyngeal symptoms after endotracheal intubation varies between 5.7% and 90%. These are usually mild and transient requiring minimal active intervention or none at all. Most resolve in 12-72 h, with an exception in cases of injury to vocal folds or arytenoids.[2] Transient hoarseness and dysphagia following endotracheal intubation is a frequent occurrence and is attributed to be a part of surgical experience, with the ensuing morbidity proportionately higher than that associated with the surgery. However, one rare complication which is distressing to the patient and the anaesthesiologist is complete voice loss following a routine endotracheal intubation. To throw more light on this subject, we carried out a search in literature including journals in English language using keywords such as 'aphonia and general anesthesia', 'voice disorders and endotracheal intubation', 'recurrent laryngeal nerve palsy' and 'general anesthesia'. The search was conducted in PubMed, Scopus, Google Scholar and Medline databases.

General anaesthesia (GA) can affect voice by interfering with the various components integral to voice production. Both laryngeal and extra-laryngeal structures may be affected. At the laryngeal level, damage to the vocal folds may be direct (secondary to a traumatic intubation with resultant oedema, haematoma, laceration or arytenoid dislocation) or indirect (with desiccation of the mucosal surface of the vocal folds secondary to inhalation of gaseous anaesthetic agents or intake of drying medications).[2]

Domino et al. inferred that the larynx was the most common site of injury in the airway for anaesthesia-related malpractice. The injuries involve vocal cord paralysis, vocal cord haematoma, intubation granulomas and arytenoid subluxation. Some of these can cause prolonged laryngeal morbidity.[3] Postoperative aphonia is a rare complication encountered in anaesthetic practice. The cause is often directly attributable to the surgery itself, as for example in head-and-neck surgeries, laryngeal surgeries or open-heart surgeries where injury to the recurrent laryngeal nerve (RLN) in the operating field is the cause. However, cases of aphonia in surgeries of distant region have also been reported where tracheal intubation itself has been the reason.[4]

 Biomechanics of Voice and Pathogenesis of Voice Dysfunction



Voice is an important tool of communication for human beings, and for some persons such as professional singers or teachers, an intact voice is extremely vital for their livelihood. Hence, any change in voice quality following a surgery under GA with airway manipulation could be catastrophic.

Voice is produced by the coordinated effort of the respiratory system (for adequate breath support), vocal cords (to bring about phonation with its fine vibratory movement), supraglottic larynx, pharynx and oral cavity (for articulation and resonance) as well as higher central nervous system functions. GA and placement of an artificial airway can affect voice production by interfering with these components.

Variations in the input of any of these areas can affect vocal cord function to varying degrees. Aeromechanical energy is initiated by the lungs, which then traverses the vocal cord structures, generating pressures and flows through constrictions. Changes in this airflow create acoustic speech. The regulation of important parameters of speech such as pitch, frequency, lingual stress and diversion of speech into various units (syllables, words and phrases) is an integral part of pulmonary function. Pain and use of neuromuscular blockers and narcotics may result in residual paralysis and postoperative pulmonary compromise after GA and may also cause changes in perceived vocal function and quality of voice.

Traumatic endotracheal intubation, irritation of posterior glottis and arytenoids due to tube motion during respiration and oropharyngeal trauma cause significant pain along the vocal tract. This discomfort results in compensatory vocal tract configurations so as to alleviate some of this discomfort, thereby causing alterations in the resonance characteristics and voice quality. Vocal fold trauma causes reactive oedema, which may result in greater vocal fold contact during the glottic cycle.

Alteration in cortical function and sensorium following the administration of narcotics, inhalational agents and neuromuscular blockers has been implicated in changes in the regularity of vocal fold vibrations and thereby the quality of phonation. Hydration of vocal fold, in terms of increase in hydration or decrease in viscosity, has shown to be associated with variations in pitch.

The vocal cords, from superficial to deep, are composed of an epithelial layer, a superficial lamina propria (made up of gelatinous glycosaminoglycans for smooth vibration of vocal cords), a vocal ligament and thyroarytenoid muscle. As a column of air travels through the airway, the cords vibrate in a smooth, periodic, co-ordinated, inferior-to-superior manner. Any oedema or inflammation of the epithelial layer or injury to the deeper layers of the vocal cords can affect the voice quality.

Changes to the vibratory characteristics of the vocal cords may occur due to several factors such as alterations in mucosal surface, abrasions from trauma due to airway instrumentation, vocal cord oedema, dehydration and increased mucosal thickness.[5],[6]

Tanaka et al. described measurable changes in the larynx following routine endotracheal intubations, namely increased airflow resistance due to intraoperative swelling of the laryngeal soft tissues.[7]

It is thus evident that vocal cord injury of varying degree occurs even with routine endotracheal intubation of short duration. It can range from hoarseness of voice, being the most common (71% of cases),[8] to the complaint of voice loss, which is a rare yet distressing complication.

 Risk Factors



Proposed risk factors for voice loss can be addressed as patient-, anaesthesia- and intubation-related risk factors.[1],[8],[9],[10]

Patient-related risk factors include age, co-morbid conditions, smoking and obesity.

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. A multivariate analysis found a threefold increased risk in those over 50 years of age.

Co-existing diseases such as diabetes, hypertension and gastroesophageal reflux disease (GERD) are also commonly implicated risk factors. Hypertension is associated with atherosclerotic changes in laryngeal vasculature. Hence, compression by the cuff can result in microcirculatory insufficiency in the nerve.[11] As diabetes is associated with peripheral neuropathy, the nerve may already be functionally abnormal at the time of intubation. This may worsen thereafter resulting in cord dysfunction.[12] Smokers are at inherent risk, whereas obese patients and patients with excessive nuchal fat deposition are known to pose difficulty in intubation.

Among the factors related to intubation and anaesthesia, increased intubation time and difficult laryngoscopy increase vocal cord morbidity. Endotracheal tube (ET) characteristics such as type and size; cuff characteristics such as design, position and pressure; and use of an introducer may be significant contributory factors.[13]

Anaesthesia-related factor that increases the risk is the use of drying agents (glycopyrrolate) and inhalational agents, both of which cause dessication of mucosal surface of the glottis.[2] Neuromuscular blocking agents cause loss of fine neuromuscular control and sensation, distorting the vocal signal.

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).[4],[14]

Possible mechanical injury includes injury to RLN and hyperextension of the neck.

Injury to recurrent laryngeal nerve

Following cadaveric dissection, Ellis and Pallister described the path of the RLN, its two branches and the relationship of these when inserting an ET and inflating the cuff in the trachea. Their study showed that the RLN divides into two branches before reaching the upper rim of the cricoid cartilage. The posterior branch innervates the posterior cricoarytenoid and interarytenoids muscles before coming into contact with the cuff. On the other hand, the anterior branch runs medial to the lamina of the thyroid cartilage, innervating the lateral cricoarytenoid and thyroarytenoid muscles. As a result of its anatomical location, it can be compressed between the ET and lamina of the thyroid cartilage by an overinflated cuff or if the cuff is inflated across the cords, resulting in neuropraxia. Thus, injury to RLN can produce paralysis of vocal cords and affects voice production. Another important consideration would be the risk of aspiration in these patients.[4]

Vocal cord paralysis is generally unilateral, compromising the left vocal cord in approximately 70% of the cases. This could be explained by the turning of the ET to the left by a right-handed anaesthetist during intubation and its fixation at the right angle of the mouth, with less chance of damage to the RLN on that side.[11],[15] There have also been reports of transient vocal cord paralysis with the use of laryngeal mask airways and double-lumen tubes.[16],[17],[18]

Hyperextension of the neck

This is thought to stretch the vagus nerve, which is anchored by the RLN in the mediastinum.[19] Haematoma and RLN palsy due to traction on the nerve have been reported in a patient who was operated in the prone position, with the head turned to the right.[20] These observations go in favour of avoiding excessive movement and turning of the neck to one side in an intubated patient.

One of the authors (KN) recalls a 32-year-old male with multiple fractures of the right upper limb, avulsion of the right scalp and facial wounds and Mallampati class II airway who was taken up for surgery at the institution where she works (unpublished data). The patient was intubated with 9.0 mm ID cuffed ET. The head had to be turned several times during scalp repair. The patient was extubated after 7 h of surgery. Voice loss was noted 2 h after extubation. Indirect laryngoscopy (IDL) on the 2nd day showed slight wavy distortion of both cords. He was managed with exercises to tone the laryngeal musculature. Over the next 60 days, the patient regained his normal voice. Repeat IDL at the 2nd and 3rd months showed gradual improvement in cord alignment. Six months later, IDL showed near-normal vocal cords.

Endotracheal tube and cuff characteristics

Several characteristics of the tube play an important role, tube diameter being one of them. Individualising the tube size for each patient would be a rational recommendation. For example, while anaesthetising a professional singer, it would be prudent to use a slightly smaller size than indicated to avoid any sort of laryngeal injury and minimise voice dysfunction in the postoperative period.[5]

The duration of intubation and number of attempts also play an important role in determining postoperative laryngeal morbidity. A 50-year-old obese, diabetic female was posted for laparoscopic cholecystectomy in the institution where the senior author (KN) works (unpublished data). The patient had a short neck with a Mallampati grade III airway. She was intubated on the third attempt with a 7.0 mm ID cuffed ET. The surgery lasted for 1 h. The patient complained of severe sore throat in the immediate postoperative period and on postoperative day 3, she developed loss of voice. IDL showed slight bowing of the left vocal cord. She regained her normal voice after 26 days.

Although the association of prolonged intubation and a myriad of laryngopharyngeal morbidities are well established, the causal relationship between prolonged intubation and vocal cord paralysis is unclear. The presence of the tube in the trachea for a long period can incite acute inflammation, erythema, ulceration and granuloma formation, which may induce cord immobility. Repeated attempts at intubation increase the likelihood of trauma to the delicate vocal cords and other airway structures. Initial and delayed true vocal cord immobility were associated with the duration of intubation and size of ET.[21]

Increased cuff pressure causes ischaemic tracheal injury. Mean cuff pressure and cuff volume are the most important factors affecting vocal characteristics. Increase in cuff volume and number of intubation attempts were found to cause vocal fatigue. A similar association between increased cuff pressure and compromised postoperative throat clearing was reported in the same study.[22]

Most authors recommend a pressure of 25-34 cm H2O on lateral tracheal wall at the end of expiration. Cuff pressure does not remain static during surgery and can increase intraoperatively due to many factors such as diffusion of nitrous oxide or oxygen into the cuff, movement of the head away from neutral position, coughing and straining on the tube due to light planes of anaesthesia.[1] Intracuff pressure is also influenced by anaesthetic depth, degree of muscle relaxation, patient temperature and position, ventilation mode and additional drug administration.[23] 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. The postulated mechanism is that the irregularly inflated or overinflated cuff presses against the larynx and compresses the RLN between the cricoid and the arytenoids, resulting in neuropraxia.[15]

One of the authors (SV) believes that the mechanism described in the preceding paragraph could have been the cause of voice loss in a 46-year-old male who was operated for the excision of intestinal stromal tumour in her institution (unpublished data). He had a Mallampati class I airway and was intubated with 8.5 mm ID ET in the first attempt. Cuff was inflated with air, and cuff pressure was not monitored. Surgery lasted for 3 h. On the 2nd postoperative day, the patient complained of hoarseness followed by loss of voice a day later. IDL revealed right vocal cord palsy. The condition resolved spontaneously with return of normal voice in 45 days. Repeat IDL at the 2nd month follow-up revealed a slightly mobile right vocal cord, with the left vocal cord compensating adequately.

The position of the cuff in the trachea is also a critical factor. It is found that the area 6-10 mm below the vocal cords is most susceptible to injury. Hence, Cavo et al. recommend that the cuff be placed at least 15 mm below the cords to avoid pressure neuropraxia.[9],[24] It has been found that positioning the cuff at or just below the vocal cord and extubating before the cuff is fully deflated cause injury to the anterior branch of RLN.[4],[8],[11] Mucosal injury from high-pressure cuffs; pressure from relatively stiff tracheal tubes on the posterior pharyngeal wall, arytenoid cartilages and vocal cords and the use of lubricant gels and topical local anaesthetic ointments are well-recognised risk factors for postoperative laryngeal problems, especially sore throat.[25]

 Surgical Considerations



Surgery along the course of the RLN can lead to vocal cord paralysis and dysphonia postoperatively. Surgery of the brainstem, skull base, neck (thyroid surgery) and chest can cause injury to the RLN along its path, and the phonic disability is easily explained. Surgeries in distant regions, especially of short duration, causing vocal cord injury are more perplexing in their aetiologies, and it is then that the anaesthetic technique and the airway management come under the scanner and warrant further analysis. Duration of surgery and anaesthesia is a critical factor, more so in surgeries lasting over 6 h.[8]

The differential diagnosis of vocal cord palsy occurring after an intubation includes arytenoid dislocation, hereditary neuropathies, synechia of processus vocalis and psychogenic paresis.[19]

Clinically, patients usually present with hoarseness of voice, voice fatigue, sore throat, raspy voice and increased throat clearing which may progress to total voice loss. Rarely, patients may present with total voice loss itself as the first complaint.[26] They may also present with stridor, apnoea and agitation in more severe cases.

It is important to assess the structure and function of the vocal cords to come to a definitive diagnosis. Diagnosis is confirmed with flexible/rigid fibreoptic laryngoscopy, electroglottography, videostrobolaryngoscopy and laryngeal videoendoscopy. Laryngeal function evaluation is performed by fundamental frequency perturbation analysis and subjective speech analysis. The latter requires two doctoral-level speech pathologists who analyse the recordings of the patients' voices. Postoperative changes are characterised by decreased intensity, reduced effect and increased roughness.[6],[27]

 Management



Most cases resolve spontaneously over days to weeks but may cause long-term morbidity.[28] Guided speech therapy and voice exercises hasten early return of functional phonation.

Medialisation procedures with injection of an inert Teflon into the paralysed cord and resection of posterior vocal cord with or without arytenoid cartilage are the treatment options in more severe cases.[29]

 Preventive Measures



As prevention is the best form of treatment, we propose a safety checklist to minimise or avoid the occurrence of this disturbing complication of voice loss following endotracheal intubation. The safety checklist may be conveniently divided into three segments - preoperative, intraoperative and postoperative. [Table 1]{Table 1}

 Conclusion



Voice loss following endotracheal intubation is a rare but alarming complication. It occurs more commonly in patients aged more than 50 years with concomitant diseases such as diabetes, hypertension and GERD with prolonged and difficult intubations. The main focus should be on prevention. Selecting an appropriate-sized ET; placing the cuff well below the vulnerable zone, at 15 mm below the vocal cords; monitoring cuff pressure and ensuring adequate anaesthetic depth intraoperatively and smooth extubation postoperatively will help in avoiding this problem. Prompt diagnosis and a coordinated multidisciplinary approach will be the cornerstone in ensuring early return to a functional social life for the patient. Well-designed randomised studies and standardised protocols using acoustic analysis both pre- and postoperatively along with voice handicap index are suggested for further research.[13][30],[31]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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