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Arytenoid subluxation after a difficult intubation treated successfully with voice therapy.

Arytenoid subluxation is a rare laryngeal injury that may follow instrumentation of the airway and present as hoarseness (1), vocal fatigue (1), stridor (2), dysphagia (1), odynophagia (3) and sore throat (1). It refers to partial displacement of the arytenoid within the cricoarytenoid joint, as distinct from arytenoid dislocation, which is complete separation of the arytenoid cartilage from the joint space. Often, cases are misdiagnosed as vocal cord paresis, laryngeal oedema or laryngospasm. (4) Knowledge of the symptoms and signs of arytenoid subluxation aids in correct diagnosis and early treatment, which is crucial for successful reduction. The aetiology, diagnosis and treatment of the condition with a review of the literature are discussed.


An 88-year-old, 60 kg male with type 2 diabetes mellitus underwent elective left inguinal hernia repair with insertion of mesh under general anaesthesia. He had no history of laryngeal disorders and no previous experience of general anaesthesia. Airway assessment revealed a modified Mallampati class 2 and slight limitation of neck extension. After being premedicated with intravenous midazolam 2 mg, anaesthesia was induced with a combination of propofol 60 mg, fentanyl 50 [micro]g and inhaled sevoflurane. After sufficient depth of anaesthesia was achieved, a laryngeal mask airway (LMA) ProSeal size 3 was placed. A poor airway seal was obtained despite repositioning of the LMA ProSeal and so tracheal intubation was attempted after administration of atracurium 30 mg and a further bolus of propofol 80 mg and fentanyl 25 [micro]g. Direct laryngoscopy (Macintosh 3 laryngoscope blade) revealed a grade 3 Cormack and Lehane laryngeal view with laryngeal manipulation. After blind passage of a gum elastic bougie into the trachea, an 8 mm Mallinckrodt endotracheal tube was railroaded over the bougie and rotated 90[degrees] anticlockwise before passing through the vocal cords. There did not appear to be any impingement of the endotracheal tube on the arytenoids during this manoeuvre. Anaesthesia was maintained with sevoflurane, nitrous oxide and oxygen. Upon completion of uneventful surgery, the endotracheal tube cuff was deflated and the trachea was extubated without difficulty.

In the recovery room, the patient was soon noted to have a hoarse voice and very loud inspiratory stridor, which was likened to a "seal grunting". There was no evidence of respiratory distress and haemoglobin oxygen saturation remained at 98 to 100% on 5 1/minute of oxygen via a Hudson mask. Auscultation of the chest demonstrated good alveolar air entry without wheezing and auscultation of the larynx revealed loud inspiratory stridor. A differential diagnosis of airway oedema, laryngospasm, vocal cord paresis and arytenoid subluxation was entertained. As haemoglobin oxygen saturation was well maintained and auscultation revealed reasonable air entry, bag and mask ventilation and intubation were not attempted. Instead, the patient was reassured and consultation with an ear, nose and throat specialist was sought. In the meantime, the patient was treated with nebulised adrenaline (2.5 mg) with no improvement. The specialist review raised the possibility of arytenoid subluxation/ dislocation as the most likely diagnosis and recommended flexible fibreoptic laryngoscopy. After explanation to the patient of the procedure and airway topicalisation, flexible fibreoptic laryngoscopy was performed, showing anteromedial subluxation of the right arytenoid cartilage associated with overlying oedema, and slight shortening of the right aryepiglottic fold. The patient was instructed to perform a simple vocal cord exercise that involved taking a vital capacity breath and forcefully phonating "eeeee" down to the residual volume. There was almost immediate resolution of his stridor after the fourth attempt. After observation for one hour without recurrent episodes of stridor, the patient was transferred to the ward from the recovery room. The patient's hoarseness persisted but resolved completely over the next 24 hours without further treatment and he was discharged from hospital on the second postoperative day.



A follow-up phone call at one week postoperatively ascertained that the patient experienced odynophagia for two days after the operation. Two weeks postoperatively, the patient attended a routine surgical outpatient appointment and was noted to be symptom-free. Two months later, a phone interview revealed no recurrence of hoarseness or odynophagia.


Korman et al first reported disruption of the cricoarytenoid joint in 1973 as a rare and unusual complication of intubation (5). A MeDLINe search of all cases to date using the search terms "arytenoid subluxation" and "arytenoid dislocation" identified fewer than 80 cases, although the true incidence is probably under-reported owing to misdiagnosis as vocal cord paresis. A prospective study suggested an incidence of one arytenoid subluxation or less for every 1000 direct laryngoscopic intubations (0.1%) (6), while a large retrospective review of 11,918 intubations revealed an incidence closer to 0.023% (7). Intubation trauma is the most common aetiologic factor cited in the literature8. The use of a LMA (9), lighted stylet (7), McCoy laryngoscope10 and double lumen tube (11), as well as cases of difficult intubation (3,12,) have been reported to be associated with arytenoid subluxation. In addition, blind instrumentation of the oesophagus with a rigid nasogastric tube and transoesophageal echocardiogram probe have also been implicated as potential factors (13). Although no disease process or anatomic abnormality has been linked definitively with an increased risk of arytenoid subluxation, there are several case reports involving patients with laryngomalacia (14), diabetes mellitus (3), chronic renal failure (3), acromegaly (4) and chronic steroid use (4). While our patient had a history of diabetes mellitus which may contribute to degeneration of the cricoartyenoid joint, it is uncertain whether this alone or in combination with a difficult intubation and/or LMA manipulation contributed to the complication.

The cricoarytenoid joint is a synovial joint enclosed by a capsule that receives posterior support from the posterior cricoarytenoid ligament. Although posterior subluxations have been reported, antero-medial subluxations predominate in the literature1 (as in our case) and involve disruption of the stabilising posterior cricoarytenoid ligament resulting in unopposed pull by the vocal cord adductor muscles, which perpetuate the subluxation. Anterior displacement is believed to occur when the arytenoid is subluxed directly by the blade of a laryngoscope as it is inserted and lifted in an anterior direction. Equally possible is a misdirected endotracheal tube tip or stylet that can simply knock into the arytenoid as the anaesthetist searches for the glottic opening. Hence, in the prevention of anterior subluxation, it would seem logical that good visualisation of the laryngeal inlet including the position of the arytenoids is important prior to instrumentation of the airway.

Where a gum elastic bougie is used, failure to rotate the endotracheal tube 90[degrees] anti-clockwise before approaching the larynx may cause impingement and trauma to the arytenoid. As this manoeuvre was performed without difficulty in our patient, we consider this mechanism unlikely. While a correctly positioned LMA should pose no Risk to the arytenoids, malpositioning of the LMA, as occurred in our case, could potentially cause damage to the arytenoids either directly or indirectly (15). Direct trauma could occur if the LMA impacts with the arytenoids during insertion, especially if the device presents a broad leading edge, while indirect trauma may occur if the tip rests in the laryngeal inlet and other forces such as cuff over-inflation pressed it into the arytenoids.

Patients with arytenoid subluxation primarily report hoarseness upon presentation (1,8.) Vocal fatigue, inability to project the voice and stridor are also common symptoms. When stridor does occur, it is unusually loud and typically can be heard some distance away. Dysphagia, odynophagia and sore throat are less common. Because of its infrequency, arytenoid subluxation may be easily mistaken for other similarly presenting conditions like laryngeal oedema, laryngospasm or recurrent laryngeal nerve paralysis from pressure on the nerve from the endotracheal tube cuff. This is compounded by the fact that symptoms of hoarseness and sore throat are common postoperative complaints after a general anaesthesia with intubation (ranging from 14.4 to 50%) (16). Nonetheless, it is important that anaesthetists remain alert for the occurrednce of this condition in order to establish the diagnosis early, because prolonged subluxation of the arytenoid may result in fibrotic ankylosis of the joint, and reduction may become impossible. If the diagnosis is suspected, a thorough laryngeal examination should be performed using a laryngeal mirror or flexible fibreoptic laryngoscope. Physical findings that suggest acute arytenoid subluxation include reduced vocal cord mobility and arytenoid oedema with loss of arytenoid symmetry. In cases where endoscopic evaluation of the larynx is obscured by oedema and haematoma, imaging techniques such as computed tomography and magnetic resonance imaging may be useful. In addition, electromyography of the laryngeal musculature is helpful in distinguishing a neurologic from a joint abnormality. In our patient, the diagnosis was alluded to by the presence of very loud, characteristic inspiratory stridor, which was recognised by one of the anaesthetists as similar in presentation to another case more than 10 years earlier.

A review of the literature indicates that the treatment of choice is surgery (4). Early treatment of arytenoid subluxation includes direct laryngoscopy and closed reduction of the subluxated arytenoid with the patient under general anaesthesia or under local anaesthesia with intravenous sedation. In general, the earlier the intervention, the better the outcome for voice quality. Where closed reduction fails or in cases of late arytenoid subluxation, a more invasive procedure known as vocal cord medialisation is preferred in order to provide adequate glottic closure necessary for vocalisation and coughing. Other modalities of treatment have been described and include chemical splinting using botulinum toxin, (9) arytenoidectomy (17) and cricoarytenoid arthrodesis. (18) Voice therapy is a non-invasive form of treatment that has been used as an adjunct to closed reduction or in patients who refuse surgical intervention. The patient is instructed to take a vital capacity breath and then forcefully phonate "eeeee" down to the residual volume. This exercise can achieve a reduction in subluxation by raising the larynx, lifting the arytenoids and causing hyper-adduction and vibration of the arytenoid hood, thereby rearranging the articulatory surface of the cricoarytenoid joint. Although its effectiveness has been questioned, it worked very well in our patient who avoided more invasive procedures and another anaesthetic. In cases involving subluxation (and less so, dislocation) of the arytenoid, we believe that the prescription of voice therapy may be a simple yet effective, low-risk and low-cost treatment option that should be tried as a first line treatment over other forms of treatment. In our experience, this is the second case of arytenoid subluxation over 10 years and in both instances the prescription of voice therapy has been successful.


Although arytenoid subluxation after a difficult intubation is a rare event, it is important for anaesthetists to be aware of its occurrence and the numerous conditions it may mimic. It is a diagnosis that should be made as early as possible in order to optimise the probability of successful reduction and restoration of normal voice. Our case highlights how this condition may be treated with simple yet effective voice therapy, obviating the need for more invasive approaches.


(1.) Sataloff RT, Bough ID, Spiegel JR. Arytenoid dislocation: diagnosis and treatment. Laryngoscope 1994; 104:1353-1361.

(2.) Chatterji S, Gupta NR, Mishra TR. Valvular glottic obstruction following extubation. Anaesthesia 1984; 39:246-247.

(3.) Quick CA, Merwin GE. Arytenoid dislocation. Arch Otolaryngol 1978; 104:267-270.

(4.) Hoffman HT, Brunberg JA, Sullivan MJ, Winter P, Kileny PR. Arytenoid subluxation: diagnosis and treatment. Ann Otol Rhinol Laryngol 1991; 100:1-9.

(5.) Korman RM, Smith CP and Erwin JR. Acute laryngeal injury with short-term endotracheal anesthesia. Laryngoscope 1973; 83:683-690.

(6.) Kambic V, Radsel Z. Intubation lesions of the larynx. Br J Anaesth 1978; 50:587-590.

(7.) Szigeti CL, Baeuerle JJ, Mongan PD. Arytenoid dislocation with lighted stylet intubation: case report and retrospective review. Anesth Analg 1994; 78:185-186.

(8.) Rubin AD, Hawkshaw MJ, Moer CA, Dean CM, Sataloff RT. Arytenoid cartilage dislocation: a 20-year experience. J Voice 2005; 19:687-701.

(9.) Rosenberg MK, Rontal E, Rontal M, Lebenbom-Mansour M. Arytenoid cartilage dislocation caused by a laryngeal mask airway treated with chemical splinting. Anesth Analg 1996; 83:1335-1336.

(10.) Usui T, Saito S, Goto F. Arytenoid dislocation while using a McCoy laryngoscope. Anesth Analg 2001; 92:1347-1348.

(11.) Mikuni I, Suzuki A, Takahata O, Fujita S, Otomo S, Iwasaki H. Arytenoid cartilage dislocation caused by a double-lumen endobronchial tube. Br J Anaesth 2006; 96:136-138.

(12.) Gauss A, Treiber HS, Haehnel J, Johannsen HS. Spontaneous reposition of a dislocated arytenoid cartilage. Br J Anaesth 1993; 70:591-592.

(13.) Niwa Y, Nakae A, Ogawa M, Takashina M, Hagihira S, Ueyama H et al. Arytenoid dislocation after cardiac surgery. Acta Anaesthesiol Scand 2007; 51:1397-1400.

(14.) Roberts D, Mcquinn T, Beckerman RC. Neonatal arytenoid dislocation. Pediatrics 1988; 81:580-582.

(15.) Brimacombe JR. Arytenoid dislocation and the laryngeal mask airway. [letter; comment]. Anesth Analg 1997; 85:463.

(16.) Mencke T, Echternach M, Kleinschmidt S, Lux P, Barth V, Plinkert P et al. Laryngeal morbidity and quality of tracheal intubation. Anesthesiology 2003; 98:1049-1056.

(17.) Tolley NS, Cheesman TD, Morgan D, Brookes GB. Dislocated arytenoid: an intubation-induced injury. Ann R Coll Surg Engl 1990; 72:353-356.

(18.) Prasertwanitch Y, Schwartz JH, Vandam LD. Arytenoid cartilage dislocation following prolonged endotracheal intubation. Anesthesiology 1974; 41:516-517.

V. Tan *, S. Seevanayagam ([dagger])

Department of Anaesthesia, The Northern Hospital, Epping, Victoria, Austral ia

* M.B., B.S., Anaesthetic Registrar.

([dagger]) M.B., B.S., F.A.N.Z.C.A., Staff Anaesthetist.

Address for reprints: Dr V. Tan, Department of Anaesthesia, The Northern Hospital, 185 Cooper Street, Epping, Vic. 3076.

Accepted for publication on March 6, 2009.
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Author:Tan, V.; Seevanayagam, S.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Geographic Code:1USA
Date:Sep 1, 2009
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