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Abstract: Case Reports |

A Woman With a Persistent Hoarse Voice and Stridor Six Months Following Esophagogastroduodenoscopy FREE TO VIEW

Samuel J. Evans, MD; Brian M. Morrissey, MD; Ken Y. Yoneda, MD
Author and Funding Information

Division of Pulmonary and Critical Care Medicine. University of California, Davis, Sacramento, CA


Chest


Chest. 2003;124(4_MeetingAbstracts):309S-310S. doi:10.1378/chest.124.4_MeetingAbstracts.309S
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INTRODUCTION:  Trauma to the cricoarytenoid joint (CAJ) represents a potentially serious albeit rare complication of upper airway instrumentation. Subluxation of the arytenoid cartilage has been reported during difficult as well as uncomplicated endotracheal intubations and extubations. To our knowledge, we report the first case of bilateral cricoarytenoid joint subluxation following esophagogastroduodenoscopy.

CASE PRESENTATION:  A 70 year old woman was referred to us for shortness of breath and wheezing. She had been well until five months prior when she underwent an elective esophagogastroduodenoscopy (EGD). For several days following the procedure the patient experienced a hoarse voice. Subsequently she noticed an inspiratory wheeze. Mild shortness of breath progressed to persistent dyspnea over the following weeks and months. Trials of antibiotics and metered dose inhalers failed to relieve her symptoms. She had a past medical history of diabetes mellitus, hypertension, chronic renal insufficiency, and coronary artery disease. She had never smoked. Physical exam was significant for a hoarse voice and inspiratory stridor. Chest X-ray showed no lesions or infiltrates. Pulmonary function testing revealed a fixed obstructive pattern with flattening of the inspiratory and expiratory limbs of the flow volume loop. Computerized tomography (CT) of the neck and thorax was normal except for abnormal vocal cord position and atherosclerosis. A fiberoptic bronchoscopy was performed which showed malpositioning of the arytenoid cartilage bilaterally. The vocal cords appeared fixed and adducted with minimal to no movement on vocalization. No endobronchial abnormalities were encountered. She was referred to a laryngologist. Repeat laryngoscopy confirmed bilateral adducted vocal cords fixed in paramedian position. No abduction was observed with sniffing. A positive cough reflex was present with arytenoid palpation. Attempts to endoscopically reduce the CAJ subluxation with a spatula were unsuccessful. She ultimately underwent laser arytenoidectomy with improvement in stridor and shortness of breath.DISCUSSION: The incidence of a unilateral CAJ subluxation is estimated to be less than 1 per 1,000 direct laryngoscopic endotracheal intubations.1 The incidence of bilateral CAJ subluxation is unknown. Forces exerted via a laryngoscope blade, endotracheal tube or other instrument have been debated to cause anterior and inferior displacement of the arytenoid cartilage. 12 Systemic diseases such as rheumatoid arthritis, sarcoidosis, Wegener’s granulomatosis and renal insufficiency may predispose the joint to subluxation.12The diagnosis is often delayed. Bilateral arytenoid cartilage fixation resembles vocal cord immobility due to recurrent laryngeal nerve paralysis and thus injuries of the recurrent laryngeal nerve (RLN) are often held responsible.3 Both CAJ subluxation and RLN paralysis may result from trauma to the larynx, and are difficult to differentiate clinically. The diagnosis is established by the clinical course and laryngeal visualization. CT, electromyography, and strobovideolaryngoscopy may help distinguish arytenoid subluxation from RLN injury.3 Reduction of CAJ subluxation using a spatula under light pressure is often successful if performed in a timely manner. However with unrecognized arytenoid dysfunction or delayed treatment, the CAJ may undergo fibrosis and ankylosis. Patients such as ours may ultimately require laser arytenoidectomy to relieve stridor and respiratory distress.

CONCLUSION:  Arytenoid subluxation is a rare complication of upper airway instrumentation and should be suspected whenever persistent hoarseness and stridor follow endolaryngeal manipulations. This is the first report implicating EGD as a potential cause of arytenoid subluxation. Early recognition is essential to avoid permanent vocal cord impairment.

DISCLOSURE:  S.J. Evans, None.

Wednesday, October 29, 2003

2:00 PM - 3:30 PM

References

Paulsen FP, Rudert HH, Tillmann BN., New Insights into the Pathomechanism of Postintubation Arytenoid Subluxation.Anesthesiology.1999;91:659–666. [CrossRef]
 
Talmi YP, et al. Postintubation Arytenoid Subluxation.Ann Otol Rhinol Laryngol105(5)1996May384–390
 
Eckel HE, et al. Management of Bilateral Arytenoid Cartilage Fixation Versus Recurrent Laryngeal Nerve Paralysis.Ann Otol Rhinol Laryngol112(2)2003Feb103–108
 

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References

Paulsen FP, Rudert HH, Tillmann BN., New Insights into the Pathomechanism of Postintubation Arytenoid Subluxation.Anesthesiology.1999;91:659–666. [CrossRef]
 
Talmi YP, et al. Postintubation Arytenoid Subluxation.Ann Otol Rhinol Laryngol105(5)1996May384–390
 
Eckel HE, et al. Management of Bilateral Arytenoid Cartilage Fixation Versus Recurrent Laryngeal Nerve Paralysis.Ann Otol Rhinol Laryngol112(2)2003Feb103–108
 
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