Evaluation of Unilateral Arytenoid Lateralization for the Treatment of Laryngeal Paralysis in 14 Cats

Introduction

Laryngeal paralysis is the failure of one or both arytenoid cartilages to abduct during inspiration, thus creating an upper airway obstruction.¹ Laryngeal paralysis may result from damage to either the recurrent laryngeal nerves or to the dorsal cricoarytenoid muscles.² Laryngeal paralysis has been well documented in dogs.^3–9 Congenital and acquired laryngeal paralyses have also been sporadically reported in cats.^10–16 Potential etiologies in dogs and cats include polyneuropathy, polymyopathy, trauma, neoplasia of the vagus nerve, and masses exerting compressive or tensile forces on the recurrent laryngeal nerves.^4,6,11,16 Oftentimes, a definitive etiology is unable to be ascertained, leaving a diagnosis of idiopathic laryngeal paralysis.

Clinical signs of laryngeal paralysis include a change in voice, coughing and/or gagging during eating, inspiratory stridor, dyspnea, cyanosis, or collapse. Diagnosis is established by demonstrating failure of one or both of the arytenoid cartilages to abduct during inspiration under a light plane of anesthesia.^2,17 Because this disease is often chronic and progressive, surgical intervention is frequently required. Several surgical procedures have been reported for the treatment of laryngeal paralysis; these include arytenoid cartilage lateralization (unilateral or bilateral), partial laryngectomy, castellated laryngofissure, permanent tracheostomy, and reinnervation.^{2,12,14,18,19} Numerous complications have been reported with these surgical techniques, including aspiration pneumonia, laryngeal webbing, surgical failure, seroma formation at the surgical site, airway reobstruction secondary to laryngeal edema, and transient Horner’s syndrome.^{2–5,10,13,14,18} Due to a lower complication rate compared to other surgical procedures, unilateral arytenoid lateralization has become the surgical treatment of choice for laryngeal paralysis in dogs.^1,4,7

To date, only one comprehensive study has examined laryngeal paralysis in cats;¹⁰ however, this study combines both medical and surgical management. Additionally, the existing study combined multiple surgical techniques such as unilateral arytenoid lateralization, bilateral arytenoid lateralization with ventriculocordectomy, and partial arytenoidectomy. The purpose of our study was to describe a series of cats diagnosed with laryngeal paralysis that were treated by unilateral arytenoid lateralization. Important to note is that this manuscript does not address potential long-term complications of the procedure.

Materials and Methods

A combined search of cats with the diagnosis of laryngeal paralysis was performed through the Veterinary Medical Database (VMDB)^a and medical records from two private referral practices from January 1986 to April 2008. Ninety-nine cats were reported to have laryngeal paralysis during this time period. Cats were included in the study if laryngeal paralysis was confirmed via laryngeal examination and subsequently treated via unilateral arytenoid lateralization. Signalment, duration and type of clinical signs, diagnostic methods and results, concurrent diseases, surgical technique, intraoperative and postoperative complications, and overall outcome were extracted from the medical records when available. Follow-up information was obtained, whenever possible, from the referring veterinarian via a mailed questionnaire or phone communication when it was not available in the medical record.

Results

Of the 99 cats diagnosed with laryngeal paralysis, 14 met the inclusion criteria for the study [see Table]. Reasons for exclusion of the remaining 85 cats included no documented surgical treatment (n=60), surgical treatment other than unilateral arytenoid lateralization (i.e., tracheostomy [n=13], arytenoidectomy [n=8], ventriculocordectomy [n=2]), or lack of a documented laryngeal examination in the medical record (n=2). Median age was 16 years (range 19 weeks to 22 years), with nine (64%) of the 14 cats being ≥15 years old. Median weight was 3.8 kg (range 1.8 to 6.6 kg), and eight (57%) of the 14 cats were male.

Clinical signs reported by owners or noted on the presenting physical examination included dyspnea (n=11), inspiratory stridor (n=7), wheezing (n=2), change in voice (n=2), lethargy (n=2), anorexia (n=2), open-mouth breathing (n=1), hind-limb weakness (n=1), and dysphagia (n=1). As described in the Table, the estimated median duration of clinical signs was 18 days (range 1 day to 1 year). Median rectal temperature on presentation was 38.2°C (range 36.6°C to 39.8°C). Two cats were hypothermic with rectal temperature of 36.6°C, and one was hyperthermic with a rectal temperature of 39.8°C. Median respiratory rate was 36 breaths per minute (range 20 to 54 breaths per minute). Concurrent diseases were seen in 11 cats [see Table]. Case no. 7 had been apparently attacked by an unknown animal 2 days prior to developing clinical respiratory signs; this cat suffered multiple bite wounds to the neck. Case no. 11 was reported to have had a head-on collision with a portable space heater 1 week prior to development of dyspnea and a change in voice.

Thoracic radiographs were obtained in 12 cats. Separate cervical radiographs were obtained in case nos. 7 and 10. Thoracic radiographs were normal in case nos. 2, 3, 11, and 12. Noted radiographic abnormalities included a mild bronchointerstitial pattern (case nos. 1, 5, 8), gas dilatation of the stomach and small bowel (case nos. 6, 7), cardiomegaly (case nos. 8, 9), air distention of the pharynx seen on lateral cervical radiography (case no. 7), narrow cervical trachea (seen on lateral cervical radiography) with poor lung inflation (case no. 10), elongated soft palate (case no. 9), sternebral luxation (case no. 7), and a thoracic mass (case no. 14). An echocardiogram was performed in case nos. 8 and 9. In both cases, right ventricular hypertrophy was found to be the only abnormality. Cervical and thoracic fluoroscopy procedures were performed on case no. 13 and showed distention of the pharynx and dorsal deviation of the sternum with increased rib excursions during inspiration and no discernible diaphragmatic movement. Because a polyneuropathy was suspected in case no. 13 based on both laryngeal and diaphragmatic paralysis, a neurology consultation was recommended; however, this was declined by the owner. It is unclear from the medical record as to why fluoroscopy was chosen over standard radiography.

A technetium scan was performed on case no. 14, which revealed a severely enlarged right thyroid gland that extended from the angle of the mandible to the thoracic inlet and into the mediastinal space. The left thyroid gland appeared normal. An echocardiogram was also performed on this cat, which revealed a mediastinal mass and pleural fluid. Cytology of the pleural fluid revealed atypical lymphocytes. A fine-needle aspirate of the mediastinal mass revealed tissue of endocrine origin. This cat subsequently underwent extensive surgery, including a median sternotomy, to allow resection of the mass in its entirety. Unfortunately, the right recurrent laryngeal nerve was entrapped within the mass and required being sacrificed at the time of surgery. Histopathology of the mass revealed multiple thyroid adenomas. Two days postoperatively, case no. 14 became dyspneic and went into respiratory arrest. A tracheostomy tube was placed, and a laryngeal examination revealed that the cat had developed bilateral laryngeal paralysis.

A preoperative complete blood count (CBC) and serum biochemical analysis were performed in all cats. The most common abnormality observed on CBC was a stress leukogram. The most common abnormality identified on serum biochemical profile was azotemia (n=6).

An electromyogram (EMG) was performed on case no. 10, which revealed denervation of the laryngeal muscles as well as abnormalities associated with the dorsal cervical vertebra musculature and appendicular muscles. Case no. 10 underwent a tracheal wash and brushing to rule out airway infection as a cause of the dyspnea; this procedure revealed mild inflammation, and laryngeal paralysis was noted. To attempt to rule out a polyneuropathy, an EMG was performed; this revealed denervation of the laryngeal muscles as well as abnormalities associated with the dorsal cervical vertebra musculature and appendicular muscles. Therefore, at the time of arytenoid lateralization, biopsies of the cricoarytenoideus dorsalis and cranial tibial muscles were obtained and revealed fibrosis and vacuolar changes, respectively, lending suspicion for a steroid-induced polyneuropathy. Case no. 10 had a history of chronic and intermittent corticosteroid administration.

Laryngeal examinations, either by direct or endoscopic means, were performed in all cats included in the study. The type (unilateral versus bilateral) of laryngeal paralysis has been summarized in the Table. Ten cats exhibited bilateral paralysis, three exhibited left unilateral, and one cat displayed right unilateral laryngeal paralysis. Case no. 8 had an elongated soft palate with epiglottic entrapment. While radiographs of case no. 9 suggested an elongated soft palate, this was not noted on laryngeal examination.

All 14 cats were treated with a unilateral arytenoid lateralization with minor variations in technique. These variations included the degree of disarticulation performed and suture placement (arytenoid to thyroid versus arytenoid to cricoid) [see Table].¹ In most cases, a single strand of polypropylene suture was placed. In case no. 4, two strands of polypropylene suture were placed. In case nos. 6 and 7, a single strand of polydioxanone suture was placed. Overall, suture size varied between 5-0 and 2-0, with a median size of 3-0.

Intraoperative surgical complications were noted in three (21%) cats and included fracture of the muscular process of the arytenoid cartilage in two cats (case nos. 6, 10) and laryngeal displacement in one cat (case no. 8) [see Table]. In case no. 10, a second passage of the suture around the soft tissues associated with the arytenoid cartilage (rather than a second passage of suture through the cartilage) resulted in adequate abduction of the arytenoid cartilage. In case no. 6, a second, deeper passage of suture through the cartilage was made, and the suture was tied, resulting in adequate abduction of the arytenoid cartilage. Intraoperative laryngeal examination of case no. 8 revealed laryngeal displacement, with the right arytenoid being displaced medially. The initial suture was cut, and a second suture was placed on the same side as the first suture, with less tension. A second laryngeal examination revealed appropriate abduction of the arytenoid cartilage without laryngeal displacement.

Postoperative complications were noted in seven (50%) cats [see Table]. Pulmonary edema, which was attributed to fluid overload, developed in two cats (case nos. 1, 12). The pulmonary edema seen in case no. 1 resolved without treatment. In this cat, a large accumulation of mucus was also noted in the endotracheal tube at extubation. A bacterial culture was performed, revealing a Mycoplasma sp. The cat was treated with antibiotics, and no recurrence of respiratory compromise was seen. Case no. 12 was placed in oxygen postoperatively and treated with furosemide^b and nitroglycerine^c paste; this resulted in gradual resolution of the pulmonary edema over the following 18 hours. A cardiac echogram was performed on this cat the day after surgery, which showed a dilated left atrium with a normal mitral valve and normal contractility. Two cats (case nos. 4, 8) developed single episodes of dyspnea postoperatively. Case no. 8 was placed in an oxygen cage, but no medications were given, and the dyspnea resolved. Case no. 4 developed dyspnea the day following surgery after jumping from its cage during examination. The dyspnea resolved with mild sedation.

All cats in this study were discharged alive. Follow-up beyond discharge from the hospital was available for eight of the 14 cats [see Table]. The estimated median duration of available follow-up was 11 months (range 3 weeks to 8 years). In case no. 4, a mild, upper airway wheeze persisted at the time of discharge but was noted to have resolved when the cat was rechecked 4 weeks later. This cat was reexamined again 2.5 years postoperatively for sneezing. At the time of the recheck, no recurrence of dyspnea was reported. Case no. 5, which exhibited mild dysphagia postoperatively, returned to normal with no reported recurrence of any respiratory problems. This cat had normal annual wellness examinations for 8 years and then was lost to follow-up. The owner of case no. 9 reported that the cat had eaten, vomited, and then acutely died. No respiratory difficulty during the 6 weeks preceding death was reported by the owner, and no necropsy was performed. Case no. 12, which had been treated for pulmonary edema 4 hours postoperatively, was rechecked 3 weeks later. This cat had also exhibited hind-limb weakness preoperatively. Thoracic radiographs were obtained and showed complete resolution of the pulmonary edema, but an enlarged left ventricle and atrium were present. The hind-limb weakness was subjectively mildly worsened, but the owner reported that the cat was gradually getting stronger at home and eating well. No further workup for the hind-limb weakness was pursued. Case no. 14 had no recurrence of any respiratory difficulties after hospital discharge; however, the cat was examined 1 year later for recurrence of the thyroid masses. Radiographs at that time also showed megaesophagus. No records were available beyond the initial examination 1 year postoperatively.

Discussion

The purpose of the present study is to describe a series of cats diagnosed with laryngeal paralysis that were treated by unilateral arytenoid lateralization. The median age of cats in this study is estimated to be 16 years, with 64% of cats being 15 years or older. This differs from a previous study that showed a median age of 11 years.¹⁰ As previously reported, no sex predilection was associated with laryngeal paralysis in this study.¹⁰ The clinical signs seen in the population of cats in our study are similar to those seen in dogs with laryngeal paralysis; the most common signs are dyspnea and inspiratory stridor.^3,18,19 While regurgitation is often reported in dogs with laryngeal paralysis, this was not obvious in any of the cats in our study.

Radiographic abnormalities previously reported in cats with laryngeal paralysis include increased soft-tissue density in the laryngeal region, megaesophagus, pneumonia, and a laryngeal mass.^10,12 Preoperative thoracic radiographs were obtained in 12 of 14 cats in our study. Additional cervical radiographs were obtained in case nos. 7 and 10. No evidence of pneumonia or megaesophagus was seen in any cat.

Previous reports of laryngeal paralysis in cats have shown primarily bilateral paralysis, with fewer cases of left-sided unilateral paralysis.^10–15 Only one previous report exists of right-sided unilateral laryngeal paralysis secondary to neoplasia of the right vagus nerve.¹⁶ In our study, 10 cats exhibited bilateral paralysis, and three displayed left unilateral laryngeal paralysis, which is similar to a previous study.¹⁰ In this series, case no. 7 exhibited unilateral right-sided laryngeal paralysis. This last cat had been attacked by an unknown animal 2 days prior to developing clinical signs. Multiple bite wounds to the neck were suffered, indicating trauma as the underlying cause of the cat’s laryngeal paralysis. Therefore, to date, no cases of idiopathic, unilateral right-sided laryngeal paralysis have been reported. The left recurrent laryngeal nerve has been hypothesized to be more susceptible to damage because of its longer course and fewer nerve fibers as compared to the right recurrent laryngeal nerve.¹⁵

In this study of 14 cases, intraoperative complications were seen in three cats (case nos. 4, 8, 10) [see Table]. In all three cases, these were minor complications that required minor revision of the surgical procedure under the same anesthetic episode, and all occurred during left-sided unilateral arytenoid lateralization. Two of these cases involved fracture of the left arytenoid cartilage. The involved cats were 17 and 5 years of age. Fracture of the arytenoid cartilage in the 17-year-old cat may have resulted from brittleness of the cartilage. In the 5-year-old cat, 2-0 suture was used (compared to 3-0 in the 17-year-old cat), suggesting that it is possible that the larger-gauge needle on the 2-0 suture may have weakened the cartilage, predisposing it to fracture. The recommended suture size for arytenoid lateralization in cats is 3-0 to 4-0.² The third cat that experienced intraoperative complications was 19 weeks of age and was diagnosed with left-sided unilateral paralysis as well as a mildly elongated soft palate with epiglottic entrapment. Laryngeal displacement occurred in this cat during surgery, but this was resolved after removing the initial suture and placing a new suture with less tension. The softness of the laryngeal cartilages in such a young animal may be more easily distorted when placing tension on the suture.

Postoperative complications reported in dogs undergoing unilateral arytenoid lateralization include pneumonia, breakdown of surgical repair, megaesophagus, gastric dilatation, seroma formation at the surgical site, persistent coughing/gagging, persistent exercise intolerance, and vomiting.^3,5 Incidence of aspiration pneumonia in dogs following unilateral arytenoid lateralization in recent studies has been reported to be between 8% and 18%.^3,5

In this study, postoperative complications were seen in seven of the 14 cats (case nos. 1, 3, 4, 5, 8, 12, 14). The development of pulmonary edema was most likely secondary to fluid overload, and thus not directly linked to the surgery itself. As in dogs, persistent coughing or gagging after eating was seen in two cats included in this study. While the development of aspiration pneumonia following unilateral arytenoid lateralization is a significant risk factor in dogs, this was not found in our study (perhaps because of the limited number of cases available). Possibly with more cases and longer follow-up, aspiration pneumonia could be seen in cats postoperatively as well.

The cause of laryngeal paralysis is often elusive, and a diagnosis of idiopathic laryngeal paralysis is made. In this study, two cats were suspected to have developed laryngeal paralysis secondary to trauma. Case no. 7 likely sustained direct trauma to the right recurrent laryngeal nerve when it was attacked. Case no. 11 was reported to have had a head-on collision with a portable space heater 1 week prior to development of dyspnea and a change in voice. The delay in development of laryngeal paralysis from the time of trauma may indicate that the nerves sustained pressure-injury secondary to swelling of soft-tissue structures surrounding the nerves.

Case no. 8 was suspected to have had congenital laryngeal paralysis based on its age at the time of presentation and the lack of any history of trauma. This cat also exhibited a mildly elongated soft palate. Soft palate elongation can interfere with movement of air through the larynx and could create respiratory distress. The elongated soft palate in this cat was not addressed surgically. The medical record is unclear as to why this was not addressed. The dyspnea did resolve after left unilateral arytenoid lateralization, suggesting that the laryngeal paralysis was the primary cause of this cat’s dyspnea. Since arytenoid lateralization increases the area of the rima glottidis, this increase may have been sufficient to allow movement of air past the elongated soft palate, resolving the dyspnea. While an elongated soft palate was noted on radiographs of case no. 9, an elongated soft palate was not noted on laryngeal examination.

Iatrogenic laryngeal paralysis was diagnosed in case no. 14. This cat developed bilateral laryngeal paralysis after having extensive surgery to remove multiple thyroid adenomas—during which the right recurrent laryngeal nerve was partially excised. It is unclear as to why the paralysis was bilateral, but iatrogenic damage is suspected since no indication of laryngeal paralysis was present prior to excision of the thyroid mass. Since no preoperative laryngeal examination was documented in this cat, laryngeal function may have been subclinically impaired prior to the original surgery, and postoperative swelling may have caused the cat to become clinical for laryngeal paralysis after the thyroid mass removal.

Polyneuropathy and polymyopathy have been associated with laryngeal paralysis in dogs.⁶ Two cats with laryngeal paralysis that developed progressive neuromuscular weakness following surgery, which resulted in euthanasia within 3 months of surgery, have been reported.¹² Three cats (case nos. 10, 12, 13) in our study showed signs suggestive of or consistent with a polyneuropathy/myopathy. Case no. 10 had an EMG performed and had biopsies of the cricoarytenoideus dorsalis and cranial tibial muscles, which showed signs consistent with a generalized metabolic myopathy/neuropathy. Case no. 12 exhibited hind-limb weakness in conjunction with laryngeal paralysis, and case no. 13 exhibited diaphragmatic paralysis in conjunction with laryngeal paralysis, suggesting a polyneuropathy/myopathy in both cats. No EMG was performed in either case to confirm a polyneuropathy/myopathy. Additional studies, in which all cats diagnosed with laryngeal paralysis also undergo an EMG, may be warranted to better clarify the frequency with which laryngeal paralysis is associated with a polyneuropathy in cats.

No definitive cause for laryngeal paralysis was found in the remaining seven cats. No signs were seen in these cats that suggested trauma, neoplasia, or a polyneuropathy as a cause. Therefore, a diagnosis of idiopathic laryngeal paralysis was made.

Follow-up, ranging from 3 weeks to 8 years, was available for eight of the 14 cases. None of these cats had recurrence of respiratory difficulties. Case no. 9 died acutely at home after vomiting while eating. Airway obstruction, secondary to vomitus, was suspected as the cause of death; however, no necropsy was performed to confirm this suspicion.

Obvious limitations of this study include its retrospective nature and small sample size. Nonetheless, intraoperative complications associated with unilateral arytenoid lateralization in cats in this study were relatively few and typically minor. Because of the small size of the arytenoid cartilages in cats, extra care may be required when placing sutures to minimize the risk of fracture of the cartilage. Since many cats that develop laryngeal paralysis are geriatric and may have impaired cardiac or renal function, careful monitoring of fluid administration may help minimize the risk of intra-operative fluid overload and subsequent pulmonary edema. In the eight cats of this study with available follow-up data, no recurrence of dyspnea was noted. Results of this retrospective study suggest that the prognosis appears good for the resolution of respiratory compromise in cats with laryngeal paralysis that are treated with unilateral arytenoid lateralization. Important to note is that the majority of the cats in this study did have some form of concurrent disease that must be considered in determining the overall prognosis.

Conclusion

Laryngeal paralysis should be considered as a differential diagnosis in any cat with dyspnea, inspiratory stridor, coughing/gagging, or a change in voice. In cats with laryngeal paralysis that have signs of a potential polyneuropathy/myopathy, a full neurological evaluation, including EMG, is warranted. Based on this small case series, unilateral arytenoid lateralization appears to be a suitable method for treatment of laryngeal paralysis in cats. Additional studies are warranted to determine the type and frequency of long-term complications.