Arytenoid Cartilage Dislocation: A 20-year Experience

Arytenoid Cartilage Dislocation: A 20-year Experience *Adam D. Rubin, †Mary J. Hawkshaw, ‡Cheryl A. Moyer, ||Carole M. Dean, and ¶Robert T. Sataloff St. Clair Shores, Michigan

Summary: Arytenoid cartilage dislocation is an infrequently diagnosed cause of vocal fold immobility. Seventy-four cases have been reported in the literature to date. Intubation is the most common origin, followed by external laryngeal trauma. Decreased volume and breathiness are the most common presenting symptoms. We report on 63 patients with arytenoid cartilage dislocation treated by the senior author (RTS) since 1983. Significantly more posterior than anterior dislocations were represented. Although reestablishing joint mobility is difficult, endoscopic reduction should be considered to align the heights of the vocal processes. This process may result in significant voice improvement even long after the dislocation. Strobovideolaryngoscopy, laryngeal electromyography, and laryngeal computed tomography (CT) imaging are helpful in the evaluation of patients with vocal fold immobility to help distinguish arytenoid cartilage dislocation from vocal fold paralysis. Familiarity with signs and symptoms of arytenoid cartilage dislocation and current treatment techniques improves the chances for optimal therapeutic results. Key Words: Arytenoid dislocation—Arytenoid subluxation—Vocal fold hypomobility—Vocal fold immobility—Vocal fold paralysis—Hoarseness— Laryngeal electromyography—Laryngeal CT—Intubation—Intubation trauma—Laryngeal trauma—Videostroboscopy.

INTRODUCTION

nerve, or from a laryngeal structural problem, such as arytenoid cartilage dislocation or cricoarytenoid joint fixation. Accurate diagnosis is critical to devising the optimal therapeutic approach. Arytenoid cartilage dislocation or subluxation is diagnosed infrequently, but it may be mistaken easily for vocal fold paralysis or paresis. If the otolaryngologist is not considering the diagnosis, he or she will probably miss it. Early diagnosis and treatment are more likely to reestablish or improve joint mobility; however, previous reports have demonstrated that a good voice result can be obtained even with late surgical intervention.1,2 The cricoarytenoid joint is diarthrodial, with a synovium-lined capsule. It is formed by the articulation of the pyramidal-shaped arytenoid cartilage and the elliptical cricoid facet. The intrinsic forces from attached laryngeal muscles and ligaments

Vocal fold immobility or hypomobility can result from injury to the recurrent or superior laryngeal

Accepted for publication September 1, 2004. From the *Lakeshore Professional Voice Center, Lakeshore Ear, Nose, & Throat Center, St. Clair Shores, MI; †American Institute for Voice and Ear Research, Philadelphia, PA; ‡Global REACH, University of Michigan School of Medicine; ||The Voice Institute, Atlanta, GA; and ¶Department of Otolaryngology-Head and Neck Surgery, Thomas Jefferson University, Philadelphia, PA. Address correspondence and reprint requests to Robert T. Sataloff, Department of Otolaryngology-Head and Neck Surgery, Thomas Jefferson University, 1721 Pine Street, Philadelphia, PA 19103. E-mail: [email protected] Journal of Voice, Vol. 19, No. 4, pp. 687–701 0892-1997/$30.00 쑕 2005 The Voice Foundation doi:10.1016/j.jvoice.2004.11.002

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provide support to the joint. The joint axis lies approximately at a 45⬚ angle from the sagittal plane and a 40⬚ angle from the horizontal plane.1,3 Although traditional teaching describes cricoarytenoid joint motion as a combination of rotating, gliding, and rocking,4 its movement is more complicated. This complex mechanism controls abduction and adduction of the true vocal folds and is, therefore, critical for protection of the airway and phonation. MATERIAL AND METHODS Subjects Sixty-three patients evaluated in our office between 1983 and 2003 were found to have arytenoid cartilage dislocation. Twenty-six of them were reported previously.1,2 Evaluation Patients suspected of having an arytenoid dislocation underwent a complete head and neck evaluation and a thorough voice evaluation including fiberoptic laryngoscopy and rigid videostroboscopy. Laryngeal electromyography (LEMG) is performed by a neurologist who is board certified in electromyography and has performed over 4000 LEMGs. A monopolar electrode tests the cricothyroid, vocalis, and posterior cricoarytenoid muscles. Treatment Patients were treated with surgery (closed reduction only, closed reduction in addition to fat, Botox (Allergan, Irvine, CA) or steroid injection, closed reduction with another procedure, open reduction), and/or voice therapy. Closed reduction is attempted on every patient who proceeded to surgery. If the patient can tolerate it, reduction is performed under local anesthesia with sedation. The patient is comfortable enough to tolerate the procedure but awake enough to cooperate with the surgeon, who monitors the patient’s voice. Anterior dislocations are reduced with a Hollinger laryngoscope. Posterior dislocations are reduced with a Miller-3 laryngoscope placed into the ipsilateral pyriform sinus.5 After successful reduction, joint stability is assessed. If there is any suspicion that the joint might redislocate after reduction of a posterior dislocation, fat lateral to the thyroarytenoid Journal of Voice, Vol. 19, No. 4, 2005

muscle or Botox into the posterior cricoarytenoid muscle is injected. For instability after reduction of an anterior dislocation, Botox is injected into the thyroarytenoid muscle. Occasionally, steroid (decadron, 4 mg/cc) is injected into the cricoarytenoid joint6 to help reduce inflammation and promote healing. Patients in whom the joint redislocates in the postoperative period may be taken back for another trial of closed reduction. When endoscopic closed reduction is not successful, or is so unstable that dislocation recurs repeatedly, an open procedure is considered. Data collection Patient charts, CT scan reports, LEMG reports, operative reports, and available strobovideolaryngoscopic examinations were reviewed retrospectively for each participating patient. Information was collected on the following parameters: side and position of dislocation (left or right, anterior or posterior), mechanism of injury, amount of time before initial treatment, treatment method, LEMG results, and voice results. EMG results were reported as a percentage of decreased recruitment. Pretreatment and posttreatment voice results were initially determined subjectively by the patient and the senior author (RTS) and documented in each chart. A result of “normal” was given if the patient felt that his or her voice had returned to preinjury quality. A result of “improved” was given if significant improvement in voice was achieved, although not to preinjury quality. Results of “slight improvement” and “no improvement” signify minimal and no improvement in voice quality, respectively. Most patients had pretreatment objective voice measures, but an insufficient number had postoperative laboratory assessment to permit meaningful analysis. Initial strobovideolaryngoscopic examinations of 41 of the 63 patients were reviewed by the authors (RTS and ADR). Presurgical and postsurgical examinations were available for 31 of 50 patients who had surgical reduction of the dislocated arytenoid cartilage. These examinations were reviewed to confirm documented voice results and analyze cricoarytenoid joint mobility. The available video examinations were reviewed in a blinded fashion, so that the reviewers were unaware of the exact

ARYTENOID CARTILAGE DISLOCATION diagnosis or the previously recorded outcome. For patients whose preoperative or postoperative videostroboscopic examinations could not be located, data were extrapolated from patient charts only. Data analyses Descriptive statistics were calculated and reported as mean ⫾ standard deviation unless indicated otherwise. Statistical analysis was performed with SPSS 11.0 for Windows (SPSS Inc., Chicago, IL). Univariate analyses of associations between clinical variables of interest were determined with chi-square tests, t tests, and analysis of variance (ANOVA). A P value of less than .05 was considered statistically significant. This study was approved for exemption status by the Institutional Review Board, Graduate Hospital, Philadelphia. RESULTS Demographics, origin, treatment, and voice result are summarized in Table 1. The mean age of the study group was 42.5 years (SD ⫽ 18.6), with patients ranging from 2 to 76 years old. There were 39 females (61.9%) and 24 males (38.1%). The most common symptom was hoarseness, followed by breathiness, volume disturbance, vocal fatigue, dysphagia, stridor, and pain. The origin of arytenoid cartilage dislocation was intubation trauma in 49 patients (77.8%), external blunt trauma in 10 patients (15.9%), and other in 4 patients (6.3%). The 4 “others” included 1 laryngeal mask anesthesia, 1 whiplash injury, 1 idiopathic, and 1 not recorded. There were 35 left-sided dislocations, 25-rightsided dislocations, and 3 bilateral dislocations. In this sample, there was no significant difference in incidence of left versus right dislocations (P ⫽ .197). There were 17 anterior, 32 posterior, and 5 complex dislocations. Three patients had both an anterior and a posterior dislocation. Direction was not recorded in 6 patients. The incidence of posterior dislocations in this sample was significantly greater than the incidence of anterior dislocations (P ⫽ .032). In the intubation injury group, there was also a significantly higher incidence of posterior versus anterior dislocations (27 vs. 14, P ⫽ .042), but no statistically significant difference in side of dislocation.

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Currently, our protocol is to obtain LEMGs and CT scans of the larynx on all patients with suspected arytenoid cartilage dislocation. In this report, 39 patients had undergone high-resolution CT scanning with 24 scans reported as displaying radiographic confirmation of dislocation. Forty-five patients underwent LEMG. The LEMGs of 38 of 45 patients showed normal innervation or mild paresis. The LEMGs of 7 patients demonstrated moderate to severely reduced recruitment patterns, which suggests a recurrent laryngeal nerve (RLN) injury that could explain the vocal fold hypomobility. All patients, however, had endoscopically confirmed dislocations. Patients who did not undergo CT or LEMG included inpatients seen and treated emergently after extubation, some patients treated before these modalities were used by otolaryngologists routinely, and a few patients who could not obtain the studies for logistical or financial reasons. Fifty of the 63 patients proceeded to surgery to treat the dislocated arytenoid cartilage. Six patients received voice therapy alone, and seven refused all treatment. Four patients underwent spontaneous reduction of their dislocations. Two of the four patients who had spontaneous reductions were undergoing voice therapy. Of the 50 patients who had surgery, closed reduction alone was performed on 35. Eleven patients needed an injection of either Botox, fat, or steroid at the initial reduction. Four patients had an additional procedure at the initial surgery, such as a mass excision, hematoma evacuation, or tracheotomy. These last four patients were excluded from any statistical evaluation of voice result. Fifteen patients underwent additional procedures beyond those performed at the initial surgery. Only five patients had additional improvement in voice, whereas the other ten had no significant change. Only 9 of the 50 surgical patients (18%) regained normal voice after the initial procedure. Closed reduction was the only procedure performed on all patients, except for one (patient 63). This patient had an immediate improvement in voice at the closed reduction, but the joint was thought to be unstable, so a lipoinjection was also performed. Five of the nine patients had preoperative LEMG. All were normal, except for a mild superior laryngeal nerve paresis in two patients. The average duration between injury and closed reduction in this group was 14.3 weeks Journal of Voice, Vol. 19, No. 4, 2005

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TABLE 1. Review of Current Cases Patient Number 1

Etiology

Symptoms

Direction

Interval to Treatment

Side

CT Report

LEMG

Treatment

Outcome

1 month

None

None

Closed reduction

Normal

nr

4 months

None

None

Speech therapy

nr Right Posterior Right

n/a 1 year

None ⫹

None None

none Closed reduction, steroid injection

Improved, spontaneousreduction No f/u Slight

nr

2 weeks

None

None

Closed reduction

Normal

Posterior Right

6 days 6 weeks

None

None

7

Intubation

nr

4 months

None

None

No change Improved Improved

Posterior Left

8 months

None

Normal

Closed reduction

Improved

Anterior Left

8 months

⫹

Normal

Closed reduction

Improved

nr

n/a

None

Normal

None

No f/u

Anterior Left

1 year

⫹

normal

Closed reduction, supraglottic web excision

Improved

Posterior Left Anterior Right

n/a n/a

⫺ ⫹

None Normal

None Speech therapy

Unchanged Unchanged

Anterior Right Anterior Right

n/a 3 days

None None

None None

None Closed reduction

Unchanged Normal

16

Hoarseness, breathiness, dysphagia Intubation Hoarseness, breathiness Intubation Breathiness, vocal fatigue Intubation Hoarseness, breathiness External trauma Hoarseness, breathiness, dysphagia, vocal fatigue Unknown Hoarseness Intubation Hoarseness, breathiness Intubation Hoarseness Intubation Hoarseness, odynophonia Intubation Hoarseness

Closed reduction Teflon injection Closed reduction

Posterior Right

N/a

⫹

None

None

17

Intubation

Anterior Left

2.7 months

⫺

Normal

Closed reduction

Improved, spontaneous reduction Improved

2

3 4

5

8 9 10 11

12 13 14 15

Hoarseness, breathiness, dysphagia

Right

Left

Right

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ADAM D. RUBIN ET AL

Posterior Left

6

Externaltrauma Hoarseness, breathiness, aspiration, pain External trauma Vocal fatigue, loss of pitch control Intubation Hoarseness Intubation Hoarseness, breathiness, stridor Intubation Hoarseness, breathiness Intubation Hoarseness

18

External trauma Hoarseness

Complex Left

10 months

⫺

Normal

19

Intubation

Anterior Right

7 months 8 months

⫹

Normal

Anterior Left

1 year 11 years 11 yrs, 2 months

20

Intubation

Hoarseness, vocal fatigue, breathiness

Hoarseness, breathiness, stridor

Mild left RLN paresis

yrs, 6 months years years years years years

Slight

Teflon injection Closed reduction CR, aryenoid adduction

Slight Improved Improved

nr Improved Improved nr Slight Improved

⫹

Normal

⫹

Normal

Partial arytenoidectomy Lipoinjection Type 1 thyroplasty Revision thyroplasty Collagen injection Complex arytenoidopexy Closed reduction Closed reduction Closed reduction Speech therapy

Slight Slight

Anterior Right

n/a

⫹

None

None

24

Intubation

Anterior Left

9 months

⫹

Normal

Closed reduction

Normal, spontaneous reduction Slight

25

External trauma Breathiness, hoarseness, loss of volume Intubation Hoarseness, loss of volume, vocal fatigue

Anterior Left

13 months 1month

⫹

Normal

Teflon injection Closed reduction

Improved Normal

Posterior Right

11 months

⫹

Closed reduction, lipoinjection

Improved

Intubation

Posterior Left

3 weeks

None

70% reduced recruitment, right RLN and SLN Mild left RLN paresis

Speech therapy, partial spontaneous reduction Closed reduction

Slight

Intubation

22

Whiplash

26

27

Hoarseness

Breathiness, hoarseness

Hoarseness

Posterior Right

12 years

Improved Improved Improved Unchanged

Improvement (Continued)

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Posterior Left

23

Hoarseness, breathiness External trauma Hoarseness

25 months 55 months 55.5 months n/a

21

ARYTENOID CARTILAGE DISLOCATION

11 13 14 16 17 20

⫺

Closed reduction, excision of vocal fold hematoma Closed reduction CR, lipoinjection

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TABLE 1. Continued Patient Number

Etiology

Symptoms

Direction

Side

28

External trauma Loss of volume, Complex Right vocal fatigue, hoarseness

29

Intubation

Hoarseness

Posterior Left

Interval to Treatment

CT Report

12 years, 3 weeks

⫹

5 weeks 2 months

⫺

LEMG Mild right SLN and RLN paresis, mild left RLN paresis 30% reduced recruitment left RLN

6 months 11 months

Intubation

Breathiness, hoarseness, air hunger, decreased volume Hoarseness, breathiness, dysphagia Breathiness, hoarseness, stridor

31

Intubation

32

Intubation

33

Intubation

34

Intubation

Hoarseness, breathiness, left otalgia Hoarseness

35

Intubation

Hoarseness

36

External trauma Hoarseness, breathiness, dyspnea, aspiration

Outcome

Closed reduction

Improvement

Closed reduction Closed reduction, lipoinjection

Slight Improved

Type 1 thyroplasty Revision thyroplasty, arytenoid adduction, cricothyroid subluxation Closed reduction

Slight Improved

Posterior Left

3 months

⫹

50% reduced recuitment left RLN

Posterior Left

2 months

⫹

Normal

Closed reduction

Improved

Anterior Left

4 years, 5 months

⫹

Normal

Left closed reduction

Slight

Posterior Right Posterior Left

2 weeks

None

Normal

Closed

Normal

Complex Left

2 weeks

None

None

Improved

Posterior Left Anterior Left Posterior Right

26 months None 11 years, 7 months 11 years, 11 months ⫹

None

Indirect closed reduction Closed reduction Closed reduction Closed reduction, fat injection

50% reduced recruitment left RLN

Improved

Improved Slight Slight

ADAM D. RUBIN ET AL

30

Treatment

Intubation

Hoarseness, dysphagia, aspiration

9 days

None

None

Closed reduction

Improved

38

Intubation

39

Intubation

40

Intubation

41

Intubation

Hoarseness, dysphagia, aspiration Hoarseness, dyspnea Dyspnea, hoarseness, decreased volume Breathiness

Anterior Right Posterior Left

2 weeks

None

Normal

Bilateral closed reduction, steroid injection

No f/u

nr

n/a

None

None

None

No f/u

Anterior Right

2 years

⫺

30% reduced recruitment bilateral RLN

Closed reduction

Improved

Posterior Right

1 year, 4 month

⫺

Closed reduction

Slight

42

External trauma Dyspnea, vocal fatigue, hoarseness

Posterior Right

2 years

Closed reduction

Normal

43

Intubation

Breathiness

Posterior Left

3 months 3.5 months

⫹

20% reduced recruitment left RLN

Closed reduction CR ⫹ lipoinjection

Improved Improved

44

Intubation

11 months N/a

⫺

Left RLN paresis

Lipoinjection Voice therapy

Improved Slight

45

Intubation

7.5 years

⫹

Normal

Closed reduction

Improved

46

Intubation

Hoarseness, Anterior Right breathiness Hoarseness, loss Posterior Left of volume, breathiness Aspiration, Posterior Left dysphagia, hoarseness, breathiness

2 months

⫹

Closed reduction, lipoinjection

Improved

47

External trauma Dyspnea, hoarseness, loss of volume

29 years

⫺

70% reduced recruitment left RLN, 30% reduced recruitment left SLN, 60% reduced recruitment right SLN and RLN Mild bilateral RLN paresis

Dilation of subglottic stenosis

Unchanged

CR, Botox

Improved

Left

Complex Right

2.5 months

Mild left RLN paresis Positive 10% reduced recruitment right SLN

(Continued)

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Posterior Left

ARYTENOID CARTILAGE DISLOCATION

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TABLE 1. Continued Patient Number 48

Etiology Intubation

Symptoms Hoarseness, breathiness, dysphagia

Direction

Side

Interval to Treatment

Anterior Left

4 months

CT Report ⫹

Intubation

Hoarseness, aspiration

Posterior Left

50

Intubation

Hoarseness, breathiness, loss of volume

Posterior Left

5 weeks

⫺

60% reduced recruitment left RLN, 30% reduced recuitment left SLN

20% reduced recruitment left RLN, 70% reduced recruitment left SLN 50% reduced recruitment left SLN, 30% reduced recruitment left RLN, myasthenia gravis

36 years 51

Intubation

Breathiness, loss of volume

Anterior Left

36 years, 5 months ⫺

Normal

37 years, 38 years 39 years 2 years

52

Intubation

53

Intubation

54

Intubation

Hoarseness, Posterior Right globus sensation Hoarseness, Posterior Left breathiness Loss of volume, Posterior Left odynophonia

⫺

20% reduced recruitment right RLN

3 years

2 weeks

None

None

18 months

⫺

30-40% reduced recruitment left RLN

Treatment

Outcome

CR, lipoinjection

Improved

Type 1 thyroplasty Closed reduction CR (in office) Closed reduction, lipoinjection, botox injection of posterior cricoarytenoid muscle Closed reduction, lipoinjection

Improved Improved Improved Normal

Closed reduction, thyroplasty Lipoinjection, excision left vocal process granuloma, partial arytenoidectomy, steroid injection Arytenoid adduction, revision thyroplasty Collagen injection Bilateral lipoinjection Closed reduction

slight

CR, lipoinjection

Improved

Closed reduction, lipoinjection Closed reduction x 2 (redislocated in PACU)

No f/u

Improved

Improved

Improved Improved Improved Improved

Improved

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49

16 months 6 months 6 months, 1 week 6 months , 2 weeks nr

LEMG

Intubation

Hoarseness, airway obstruction Hoarseness, breathiness, odynophagia Hoarseness, odynophagia, loss of volume Hoarseness, breathiness, diplophonia, loss of volume

Complex Left

1 day

None

Closed reduction, trach

n/a

None

30-40% reduced recruitment bilateral RLN Normal

56

Intubation

Posterior Right

6 days

Closed reduction

Improved

57

Intubation

Posterior Left

3 weeks

None

Normal

Closed reduction

Normal

58

Intubation

Posterior Right

2 weeks

None

Closed reduction, lipoinjection

Improved

Stridor, hoarseness Hoarseness, breathiness, vocal fatigue, loss of volume Hoarseness

Anterior Left

3 days

None

60% decreased recruitment right RLN, 20% reduced recruitment right SLN None

59

Intubation

Closed reduction

Normal

60

Idiopathic

Posterior Left

2 years

⫹

70-80% reduced recruitment left RLN and SLN

Closed reduction, lipoinjection

Improved

61

Intubation

Posterior Right

23 years

Closed reduction, lipoinjection

Slight improvement

Breathiness, loss of volume, vocal fatigue

Anterior Right

5 years

⫺

Voice therapy

No improvement

Posterior Left

2 months

⫹

20% reduced recruitment right RLN and SLN, 80% reduced recruitment left RLN (diagnosed and treated with Teflon injection years ago by other otolaryngologist), 30-40% reduced recruitment left SLN 30-40% reduced recruitment right RLN, 10–20% reduced recruitment left RLN, 10% reduced recruitment bilateral SLN (history of Guillan-Barre) 20% reduced recruitment left SLN

62

Intubation

63

LMA intubation Hoarseness, breathiness

Closed reduction, lipoinjection

Normal

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Abbreviations: nr, not recorded; n/a, not applicable; RLN, recurrent laryngeal nerve; SLN, superior laryngeal nerve; CR, closed reduction; f/u, follow-up.

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(SD ⫽ 33.7). However, if we exclude the outlier (patient 42), the average was 3.1 weeks (SD ⫽ 2.7). Twenty-seven patients (54%) had significant voice improvement after initial surgical intervention, but they did not return to their preinjury voices. Closed reduction was the only procedure performed on 19 of the 27 patients as initial surgery. Seven patients had closed reduction with an injection, and one patient had closed reduction and excision of a supraglottic web. Twenty-two patients in this group had preoperative LEMG. Eight were normal, whereas 14 showed some abnormality. Six of the seven patients who required an injection had at least 50% reduced recruitment in the ipsilateral RLN. Of the seven patients with abnormal LEMGs who had closed reduction alone, only one patient had a 50% reduced recruitment of the ipsilateral RLN. The other six had milder paresis of the ipsilateral or contralateral RLN or superior laryngeal nerve (SLN). The average time from injury to initial treatment in this group was 95.5 weeks (SD ⫽ 167.7), with a range from 6 days to 12 years. Seven patients from this group had additional surgical procedures later, with one obtaining a normal voice. Ten surgical patients (20%) experienced only slight voice improvement. Six of the ten had closed reduction alone, two required concurrent injections, and two had other procedures at the initial surgery, including a tracheostomy and an excision of a vocal fold hematoma. Five of the ten patients had normal LEMGs. Of the other five EMGs, only two demonstrated more than a mild paresis. One patient requiring fat had an old contralateral paralysis and had had a previous Teflon injection by another otolaryngologist. The average time interval between injury and initial surgery was 415 weeks (SD ⫽ 637) in this group with a range from 5 weeks to 36 years. Five patients from this group had additional surgical procedures later. Three had significant improvement.

Two patients had no voice improvement after initial surgical intervention. Airway obstruction was the primary problem with one patient; thus surgery was performed to open and secure a safe airway, compromising voice result. The other patient did not have a preoperative LEMG or a CT scan. That patient had significant improvement with injection laryngoplasty performed later. Two surgical patients were lost to follow-up. Of the six patients who had voice therapy alone, three had no improvement, two had slight improvement, and one had significant improvement. Two patients had some degree of spontaneous reduction apparent on strobovideolaryngoscopic examination. Of the seven patients who refused all therapy, two had spontaneous reductions resulting in a normal voice in one and a significant improvement in the other. Two patients had slight improvement in voice over time, and three were lost to follow-up. One-way ANOVA was performed to compare time to surgical treatment across the voice improvement groups. The four patients who had additional, nonrelated procedures (eg, excision of vocal fold hematoma, tracheostomy) were not included in this analysis. Those whose voices returned to normal (n ⫽ 9) averaged 14.3 weeks to treatment (SD ⫽ 33.7), those whose voices showed significant improvement (n ⫽ 25) averaged 97.2 weeks to treatment (SD ⫽ 170.9), those whose voices showed slight improvement (n ⫽ 8) averaged 279.9 weeks to treatment (SD ⫽ 422), and the one whose voice showed no improvement was treated within a week of the injury. Although a trend suggests worse voice results with increased time to surgical intervention, overall ANOVA was not significant (P ⫽ .105) (Table 2). Neither the mechanism of injury nor an abnormal EMG had a significant impact on treatment outcome. However, patients with ⬎50% reduced recruitment

TABLE 2. Voice Result Compared With Time to Treatment (n ⫽ 44) Voice Result Time to treatment (Weeks ⫾ SD)

Normal (n ⴝ 9)

Improved (n ⴝ 26)

Slightly Improved (n ⴝ 8)

No improvement (n ⴝ 1)

14.3 ⫾ 33.7

97.2 ⫾ 170.9

279.9 ⫾ 422

1

Note: Although a trend suggests that voice results may be better with earlier treatment, ANOVA was not significant (P ⫽ .105). Abbreviation: SD, standard deviation. Journal of Voice, Vol. 19, No. 4, 2005

ARYTENOID CARTILAGE DISLOCATION of the ipsilateral RLN were significantly more likely to require fat or steroid injection than were those without such a severely abnormal LEMG (P ⫽ .001). Of the 41 patients whose strobovideolaryngoscopic examinations were available for review, 25 had no preoperative movement, 15 had some preoperative movement, and the strobe of 1 patient could not be adequately evaluated because of severe supraglottic hyperfunction. The correct diagnosis for direction and side of dislocation was made in all but three patients. One was a patient with severe hyperfunction, which made assessment difficult. In another, the joint was hypermobile, and the height of the vocal process fluctuated. The third patient suffered a complex dislocation, rather than the classic anteromedial or posterolateral dislocation. Of the 31 patients whose postoperative examinations were also available, only 6 demonstrated improved movement of the affected joint. Four of the six patients (patients 8, 33, 45, and 63) had an immobile joint preoperatively. The other two (patients 25 and 60) had some preoperative movement. The increased mobility was initially noted on stroboscopy from 3 weeks to 3 months postoperatively in all but one of the six patients. That patient did not follow up until 9 months after surgery, when restoration of movement was noted. The interval between treatment and injury for these patients was 2 weeks to 7.5 years. All patients had normal EMGs, except for number 63, who had a mild ipsilateral superior laryngeal nerve paresis. Half of the patients with improved mobility regained a normal voice, and the other half had significant voice improvement. DISCUSSION Not including the patients reported in this study or previously by the senior author (RTS), 74 cases of arytenoid cartilage dislocation are reported in the literature.7–31 The actual incidence is most likely higher than the literature reflects, because many are misdiagnosed as vocal fold paralysis. This study involves the largest number of cases reported to date. The most common etiologic factor of arytenoid cartilage dislocation cited in the literature is intubation trauma (59 of 74 cases, 80%), followed by external trauma, accounting for 15%. The remaining

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5% includes other causes such as laryngeal mask anesthesia and gastroscopy. Our series supports these findings, with 49 of 63 (77.8%) patients exclusively having intubation trauma. External neck trauma was found to be an etiologic factor in 11 patients (17.4%). The symptoms in one patient developed when she experienced numerous violent coughing episodes caused by bronchitis. Although LEMG demonstrated evidence of paralysis, endoscopy showed dislocation of the joint. Whether the dislocation resulted from excessive coughing or as a result of the paralysis is unclear. Several theories attempt to explain how the arytenoid cartilage can become dislocated as a result of intubation. In general, these theories postulate that the arytenoid cartilage is directly traumatized from the laryngoscope, the endotracheal tube or stylet, or an incompletely deflated tracheal cuff.11,13,16 Paulsen et al32 suggested that dislocations might not occur directly by knocking the arytenoid out of place. Rather, they postulate that trauma to the joint results in hemarthrosis and scarring, which subsequently lead to abnormal positioning of the joint. We have observed significant scarring and hemarthrosis in dislocated joints in the few patients in whom we had to perform open reduction. Whether this finding ultimately is the cause or the effect of the dislocation is unclear. Although the exact mechanism remains unknown, we believe that posterior arytenoid dislocations result from trauma during extubation, and anterior arytenoid cartilage dislocations occur during intubation. Wang3 performed selective sequential disconnection of muscular and ligamentous structures to identify the stabilizing forces on the cricoarytenoid joint. He determined that the vocal ligament, conus elasticus, and anterior capsular ligament resisted posterolateral displacement of the larynx, whereas the cricoarytenoid ligament and posterior capsular ligament prevented anteromedial displacement. He concluded that significant forces are necessary to disrupt the major support structure of the cricoarytenoid joint and produce subluxation in a normal larynx. Several authors have suggested that arytenoid cartilage dislocation occurs only when the joint is compromised by systemic disease, such as acromegaly or renal failure.8,9,11,13,16 In our study, however, most patients had no underlying chronic diseases. Journal of Voice, Vol. 19, No. 4, 2005

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Typically, posterior dislocations result in a posterolateral displacement of the arytenoid cartilage, whereas anterior dislocation results in an anteromedial displacement of the arytenoids. Ascertaining the direction of dislocation is difficult, but critical, because it will affect the technique of reduction. Over half of the reports in the literature do not specify the direction of dislocation. Rigid stroboscopy is invaluable in determining the direction of dislocation. One should focus on the height disparity between the vocal processes and the length of the vocal fold. A posteriorly dislocated arytenoid results in a high vocal process and a stretched vocal fold. An anterior dislocation results in a low vocal process and a short vocal fold. The position of the apex of the arytenoid can be deceiving and is not a reliable indicator of direction of dislocation. A less common dislocation involves an anteriorly dislocated arytenoid, rotated so that the vocal process is high. We call this a “complex” dislocation. Although the literature suggests that anterior dislocations are more common, we observed more posterior dislocations. This observation is not surprising because the anatomy provides much less protection against posterior displacement than against anterior dislocation, possibly because all natural movements and forces tend to pull the arytenoid cartilage anteriorly. The most common presenting complaint in both the literature reviewed and our current series was hoarseness,which commonly describes various symptoms, and most patients also have prominent breathiness and decreased volume. Odynophagia was less commonly reported in our study population than in the literature. We tend to see patients further out from the injury. Thus, patients might have had odynophagia or pain initially, but they do not report it because it has resolved by the time we evaluate them. However, sore throat and hoarseness are common postoperative complaints after general anesthesia, involving approximately one third to one half of patients after intubation. Traumatic laryngitis usually resolves within 3 days without treatment. When symptoms persist for longer than 1 or 2 days after surgery, or when hoarseness is severe, an otolaryngologist should be consulted expediently. The usefulness of CT imaging13,14,16,21,26,28 and laryngeal EMG16,26 to otolaryngologists has been Journal of Voice, Vol. 19, No. 4, 2005

touted in the literature. Alexander et al28 demonstrated that helical CT was positive in 11 patients they studied with confirmed arytenoid dislocation. Although we believe that laryngeal CT can be a useful adjunctive study in suspected cases of arytenoid dislocation, it has limitations. In young patients, the cartilage is frequently not ossified and, therefore, difficult to assess. Moreover, one needs high-quality images with fine cuts and reconstructed images of the larynx, which are not available everywhere. We believe that, although a positive CT scan is helpful to confirm the diagnosis, a negative scan does not rule out dislocation. CT scanning is useful in the setting of external trauma to look for other cartilaginous injuries that might require intraoperative repair. The relationship between the arytenoid and the cricoid cartilages is the most important feature.21 The cricoid facets and arytenoid cartilages are symmetrical in individual larynges.33 Asymmetry in the joint space, specifically obliteration or widening, supports the diagnosis of arytenoid cartilage dislocation (Figure 1). The widened joint space is usually filled with soft tissue density from hemarthrosis and fibrosis. Of course, joint fibrosis from another process, such as rheumatoid arthritis or severe laryngeal

FIGURE 1. CT scan of larynx with left arytenoid cartilage dislocation. Compare the obliterated left joint space (thick arrow) with the intact joint space on the right (thin arrow).

ARYTENOID CARTILAGE DISLOCATION reflux, might look similar on CT scan, but an adequate history and serologic studies should help determine the true etiology. Asymmetry in vocal fold height on the CT scan may be present in vocal fold paralysis; however, the joint space should be normal, unless there is a concurrent subluxation. Some speculation has occurred that joint fibrosis could result after longstanding vocal fold paralysis.21 This conclusion is controversial, however. Passive movement from contact with the mobile arytenoid cartilage (which results in the “jostle” sign) should prevent this in most cases. Only 62% of the CT scans obtained in this series were read as positive by the radiologists. We did not review the scans at the time of this study, although they were all reviewed contemporaneously. In many cases, the quality of the images was insufficient for diagnosis. In some, the laryngeal cartilages were ossified inadequately for visualization. Laryngeal EMG is helpful in distinguishing a neurologic from a joint abnormality as the origin of a hypomobile or immobile vocal fold. It, too, however, has its limitations. As we saw in our data, 25 patients (39.7%) had abnormalities on EMG. Seven patients (4.8%) had 50% or greater reduced recruitment in the ipsilateral RLN, which could explain the hypomobility. It is possible for both denervation and a joint dislocation to be present. The process of intubation and pressure from the endotracheal cuff certainly can injure the recurrent laryngeal nerve near its entrance into the larynx. In addition, the proximity of the cricothyroid joint to the cricoarytenoid joint leaves the nerve susceptible to inflammatory mediators that might be present after trauma. However, it is also possible that hematoma and scarring in the posterior portion of the thyroarytenoid muscle can appear as denervation on the EMG. Sampling different parts of the muscle should help avoid this confusion.26 The LEMG findings must be evaluated in the context of findings on rigid stroboscopy. For example, if there is dramatic asymmetry in vocal process height without a jostle sign, there is probably a structural problem in addition to, or despite, the LEMG findings. Yin et al26 report that the LEMG has prognostic implications as to the surgical results of arytenoid cartilage dislocation. Our data seem to agree with this finding. Although we did not find a statistically

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significant difference, most likely because of the small numbers involved, all patients who achieved normal voice results had essentially normal LEMGs (two mild SLN pareses). Also, patients who required simultaneous injections were more likely to have over 50% reduced recruitment in the ipsilateral RLN, probably because the arytenoid cartilage is more likely to be unstable with a significant concomitant vocal fold paresis because many intrinsic stabilizing forces on the joint would be absent. One could argue that the diagnosis of arytenoid cartilage dislocation was incorrect in patients in our series with significantly abnormal LEMGs who required injections. However, passive joint hypomobility was confirmed in the operating room. Furthermore, the voices of most patients improved immediately in the operating room with closed reduction alone (under local anesthesia with sedation, so the voices could be tested). Injection is used by the otolaryngologist only if the joint feels unstable to try to prevent redislocation, not necessarily for the medialization effect. Lastly, only 11 patients required injection at the time of the closed reduction. The most important tool for diagnosing arytenoid cartilage dislocation is strobovideolaryngoscopy. The magnified view provided by rigid stroboscopy is useful to otolaryngologists in identifying a jostle sign, looking for flickering of muscle activity that suggests an intact nerve supply, and looking for coexisting pathology, such as hematoma, scar, or mass lesions. As mentioned above, stroboscopy helps identify vocal process height discrepancies. Although there might be vocal process height discrepancies with paralysis, this is less common and usually less severe. Hong and Jung34 demonstrated that, in cases of lateral paralysis, there is usually no height discrepancy between the vocal processes, distinguishing this from posterolateral dislocation. In paramedian paralysis, occasionally there is a discrepancy, although the vocal process can be high or low compared with the innervated side. Of course, in paralysis, the stability of the joint is decreased because of the loss of tone of the laryngeal muscles. This loss leaves the joint susceptible to subluxation. We believe that, with an obvious discrepancy between vocal process heights, one must strongly consider the possibility of dislocation. Regardless, the height discrepancy must be corrected to optimally improve voice quality. Journal of Voice, Vol. 19, No. 4, 2005

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Occasionally, arytenoid cartilage dislocation leads to a hypermobile joint. In this case, the vocal process of the affected arytenoid cartilage can fluctuate between higher and lower than the contralateral arytenoid cartilage with phonation. In this setting, the joint is difficult to stabilize. Equalizing the heights of the vocal processes is the most important aspect of improving voice in arytenoid cartilage dislocation. Of the 31 examinations reviewed of patients with preoperative and postoperative videos available, movement was improved in only 6 of them. It is difficult and uncommon to restore mobility after the joint is disrupted. However, normal voice or significantly improved voice can be restored with closed reduction improving the height discrepancy between the vocal processes; this explains why good voice results can occur with closed reduction alone even years after injury, although increased scarring and ankylosis may make it more difficult to reposition the joint. Techniques of closed reduction have been previously described.5 Care must be taken not to fracture the vocal process at its fusion plane with the body of the arytenoid cartilage during reduction of an anterior dislocation. Open procedures include Type I thyroplasty, arytenoid adduction/rotation, and arytenoidopexy, among others.8,15,25,31,35 Botox has also previously been described in the treatment of arytenoid dislocation.29 Occasionally, more creative reduction techniques are warranted. For example, the author (RTS) has used a right-angle bayonet forceps with the tip covered by a red rubber catheter to reduce a posterior dislocation in a patient in the immediate postoperative period after an anterior cervical fusion. That patient had a short, thick neck and was flexed in a halo and on full dose of coumadin. In other cases, the author (RTS) has used digital reduction in the office and the intensive care unit with success. Spontaneous reduction of the dislocated arytenoid cartilage has been reported14,23,24 and was observed in four patients in this series. Spontaneous reduction can be preceded by coughing or vomiting. Spontaneous reduction is uncommon, however, and surgical intervention should be offered in most cases. Voice therapy is advocated for all patients. Preoperative voice therapy is particularly useful to otolaryngologists in longstanding dislocations, Journal of Voice, Vol. 19, No. 4, 2005

when immediate reduction is no longer as critical. Voice therapy can help rid the patient of poor compensatory mechanics that might cause further damage to the laryngeal apparatus, and it can occasionally provide enough voice improvement that the patient wishes to avoid surgery. The data certainly suggest that time to surgical treatment might have prognostic significance for patients with arytenoid cartilage dislocation. Although ANOVA was not significant comparing time to treatment and voice result, this could be a result of the small sample size. Future studies with larger sample sizes would not only help to clarify some of the results of this study, but would also allow for multivariate analyses that might help determine the effects of several distinct variables at the same time. Other potentially limiting factors of this study were our inability to locate and review in a blinded fashion the actual videostroboscopic examinations of almost half of the patients and the lack of objective measures we used in the study. We had to rely on previously documented information from patient charts or data previously reported on earlier patients.1,2 However, our voice assessments for patients whose stroboscopic examinations we could review agreed with assessments previously documented. Of course, additional data, such as qualityof-life measures or objective voice analysis, might have ameliorated some of these issues. CONCLUSIONS The diagnosis of arytenoid cartilage dislocation should be considered in all cases of vocal fold hypomobility and immobility. Videostroboscopy is the most critical part of the examination, although laryngeal CT and EMG are useful to otolaryngologists. An attempt at endoscopic reduction should be considered even when diagnosis has been delayed. Equalizing the heights of the vocal processes might improve the voice even without return of joint mobility.

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