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Arytenoid Cartilage Necrosis

1996; Lippincott Williams & Wilkins; Volume: 83; Issue: 5 Linguagem: Inglês

10.1213/00000539-199611000-00038

1526-7598

Sibylle Brosch, Roland Ripberger, H. S. Johannsen,

Phonetics and Phonology Research

As reviewed by Burns et al. [1], prolonged endotracheal intubation (in excess of 24 hours) was first described in 1880 by William MacEwen. Subsequent voice disorders and/or respiratory distress has been well documented. In most cases, injuries can be verified by microlaryngoscopy and microstroboscopy. For microstroboscopic examinations of laryngeal function, an electrically triggered intermittent discharge tube is used as the standard light source which analyzes sound from a laryngeal lowpass microphone. The method enables the viewer to see an apparently slowed sequence of vocal fold movements (the mucosal wave). Less commonly, electromyography or computed tomography (CT) is required [2,3]. The following case presentations describe arytenoid cartilage necrosis in two patients as a result of prolonged endotracheal intubation. An axial CT cut at the level of the upper portion of the arytenoid cartilages (Figure 1) demonstrates normal anatomy in this region.Figure 1: Computed tomography scan demonstrating pyramidically shaped arytenoid cartilages of regular size and their relationship to the vocal cords (the right arytenoid cartilage is indicated by the smaller arrow; the right vocal cord is indicated by the larger arrow) in a normal larynx of an 88-yr-old female.Case 1 A 34-yr-old man was seen with hoarseness to the point of aphonia. He had suffered multiple injuries in a road traffic accident 13 yr before, after which he spent 6 mo in hospital. The larynx had not been damaged during the trauma. He required a tracheostomy after several days of endotracheal intubation. Hoarseness had been present since extubation. The patient had consulted several physicians before we saw him for consideration of arytenoid cartilage mobilization. Microlaryngoscopy showed that the left vocal cord was fixed in the median position and the right was slightly mobile between the median and the paramedian position, with both vocal processes turned inward. Breathing was impaired to such an extent that it was not possible to restore medial position of the right vocal cord to improve the voice. Owing to his aphonia and thus absence of the mucosal wave, microstroboscopic examination was not possible. Normal patterns of electromyographic activity could be obtained from electrodes inserted intralaryngeally into the vocalis muscles. This excluded paralysis of the vocal cords and made ankylosis of the cricoarytenoid joints a more likely explanation for the immobility. Direct laryngoscopy under general anesthesia was performed in an attempt to mobilize the left arytenoid cartilage (long arrow in Figure 2). Only a small part of each arytenoid cartilage was preserved, without any connection to the cricoid cartilage.Figure 2: Computed tomography scan before performing extended left-sided rest-arytenoidectomy demonstrating bilateral reduction of cartilaginous mass in the arytenoid region, mainly in its medial part (arrows). Asymmetry in the computed tomography scan is partly due to the poor quality of the illustration, having thus led to the incorrect preoperative interpretation of cricoarytenoid ankylosis.An extended, left-sided "rest-arytenoidectomy" was performed in order to improve the respiratory situation. After this, during a second-stage operation, we implanted Teflon paste in the left vocal cord to allow apposition in the anterior two thirds of the vocal cords and hence close the glottis and improve the voice. This was successful. Case 2 A 61-yr-old female was found unconscious after a suicide attempt with alcohol and benzodiazepines. She was tracheally intubated and required artificial ventilation for 2.5 days. Additionally, gastric lavage was performed upon her arrival in the intensive care unit. On admission on a general ward, she complained of hoarseness and dysphagia, which had been present since extubation, followed by progressive shortness of breath and inspiratory stridor. Indirect microlaryngoscopy revealed severely edematous vocal cords. Her respiration improved after intravenous injection of 500 mg corticosteroid and inhalation of epinephrine. As laryngitis was suspected, antibiotics were started intravenously. Microlaryngoscopy 8 days later showed both vocal cords to be restricted in mobility. The patient was seen 20 wk later in our department with persistent hoarseness. Microlaryngoscopy revealed that both vocal cords were almost completely immobile in the paramedian position with posterior positioning of the arytenoid cartilages. A diagnostic CT scan demonstrated overall reduction of both arytenoids (Figure 3).Figure 3: Diagnostic computed tomography imaging 5 mo after endotracheal intubation demonstrating a large lesion in the arytenoid region with an almost complete loss of cartilaginous tissue on the left side (arrow). Restriction of vocal cord mobility has led to severe airway narrowing.Despite efforts at improving the patient's voice, it was not feasible to bring one vocal cord into medial position owing to the risk of respiratory decompensation. The patient did not give her consent to a treatment as described in Case 1, so voice therapy was started. This ended after 50 sessions, by which time her voice had improved considerably. Discussion These two case reports show severe damage to the arytenoids that we interpret as being caused by prolonged endotracheal intubation. In the first case, damage was revealed by direct laryngoscopy and rest-arytenoidectomy. In the second case, a diagnostic CT scan clearly demonstrated severe cartilaginous loss on both sides, which, as a consequence of gastric lavage, seems very unlikely. There was no history of aspiration in this patient. Dysphagia, however, can be interpreted as a result of the vulnerated arytenoid region, representing the medial limitation of the entrance to the esophagus. Arytenoid cartilage necrosis has never been referred to as such in the literature. However, when an arytenoid cartilage has been ulcerated as a result of prolonged endotracheal intubation, surely it may heal in some cases with a defect of the cartilaginous mass. In 1992, Kopp et al. [4] retrospectively studied 68 patients who had been examined by direct laryngoscopy when they were still tracheally intubated. In all cases, edema of the vocal cords was evident. In 24%, the lesion was classified as a cartilage ulcer on the arytenoid. Very rarely, ankylosis or (sub)luxation of the cricoarytenoid joint is reported as causing permanent voice disorders after endotracheal intubation [5-9]. There may of course even be interrelationships between ankylosis and minor degenerative changes of the arytenoids due to atrophy of tissue. Ulcers, however, are mainly superficial so the tissue is likely to be restored morphologically and functionally, while necrosis marks an irreversible loss of tissue and thus function. Further studies hopefully will reveal more data on the incidence of arytenoid cartilage necrosis within the spectrum of hoarseness after endotracheal intubation.