Epiglottic entrapment is an anomaly that is traditionally known as an equine syndrome (Boles et al., 1978). Similar conditions such as epiglottic retroversion as well as brachycephalic airway syndrome are reported in dogs, and nasopharyngeal stenosis and polyps are reported in cats (Kuehn, 2006; Phillips, 2022). The epiglottis is a cartilage that is part of the larynx. It is anchored to the hyoid bone by the hyoepiglottic muscle. In its normal position, the epiglottis is caudal to base of the tongue and rests ventral to the soft palate. During a nasal breath, the soft palate relaxes and moves ventrally where it may transiently contact the rostral most tip of the epiglottis (Hudson & Hamilton, 2010). In equine epiglottic entrapment, the epiglottis is obscured ventral to the arytenoepiglottic fold, and this leads to cough, exercise intolerance, loud respiratory sounds and upper airway obstruction. The aetiology is thought to be secondary to congenital hypoplasia and deformity of the epiglottis predisposing to entrapment (Boles et al., 1978). The current report describes the management of a cat with clinical signs and findings on necropsy that are very similar to epiglottic entrapment reported in equine species.
CASE SUMMARYA 5-month-old, 1.8 kg, male neutered Russian Blue cat was referred to a specialty veterinary hospital for the evaluation of suspected upper airway abnormalities. The cat initially was presented to the emergency service at a specialty veterinary hospital the previous day for acutely prolapsed nictitans of the left eye. The owners noticed the prolapsed nictitans after briefly leaving the cat alone. There was no known trauma. They also described chronic ‘snorting’ when eating and sleep-disordered breathing that seemed to be subtly improved recently.
The owners had obtained the kitten from a local breeder 3 months ago. The kitten had undergone a full series of core vaccines and routine deworming with the referring veterinarian. During all three recorded routine wellness visits, owners had expressed similar concerns for nasal congestion, abnormal sounds during eating and snoring. Owners reported that the cat would ‘choke’ on any food that was not ‘pâté’ consistency and that they were advised not to feed hard kibble by the breeder for the same reason. Wellness physical examinations were reportedly normal except for increased upper airway/stertorous breathing sounds documented at each visit. The differentials for these clinical signs included feline viral rhinotracheitis or conformational/congenital abnormalities. The kitten was treated symptomatically with over-the-counter lysine supplementation, and a sedated upper airway exam was recommended to be performed during neuter at 6 months of age.
On physical examination by the emergency service at a specialty care facility (the day prior to planned neuter), vitals were normal. There was audible upper airway congestion and stertor, no nasal discharge and normal auscultation. Ocular examination revealed unilateral miosis, protruding nictitans and hyperaemia of the left eye. The cornea and anterior chamber were clear, and there was no ocular discharge. Full fundoscopic exam was not performed. Fluorescein stain was negative for uptake in both eyes. The cat was treated supportively for presumed viral upper respiratory infection and secondary uveitis with ofloxacin ophthalmic suspension (1 drop, OS, q12h) and l-lysine paste supplementation (one-fourth teaspoon, PO, twice daily).
The following day, the cat was presented to its primary care veterinarian for recheck and new onset of lethargy as well as the development of horizontal nystagmus and ataxia. On physical examination, vitals were normal, and the cat had a horizontal nystagmus with the fast phase to the right. The left pupil was miotic with elevated third eyelid and mild enophthalmos. No abnormalities were found during otic examination of both ears. The cat had a mild vestibular ataxia with left head tilt (reportedly more prominent at discharge, post-anaesthesia). Preanesthetic diagnostics performed included an in-house complete blood count that showed a neutrophilic leucocytosis (white blood count 32.21 × 109/L (32.21 × 103/μL [RI 5.5 – 19.5 × 109/L]), neutrophils 30.47 K/L × 109/L (30.47 × 103/μL [RI 2.5 – 14.0 × 109/L]), lymphocytes 1.01 × 109/L (1.01 × 103/μL [RI 1.5 – 7.0 × 109/L]) and mild thrombocytopenia (162 × 109/L (162 × 103/μL [RI 300 – 800 × 109/L])). Serum chemistry showed mild hyperglycaemia (glucose 9.657 mmol/L [174 mg/dL), RI 4.27–8.5 mmol/L (77–153 mg/dL)], mild decreased blood urea nitrogen [0.49 mmol/L (9.0 mg/dL), RI 0.88–1.83 mmol/L (16–33 mg/dL)) and creatinine [0.027 mmol/L (0.5 mg/dL), RI 0.033–0.088 mmol/L (0.6−1.6 mg/dL)) but was otherwise unremarkable. Rapid immunoassay screening for feline immunodeficiency virus and feline leukaemia virus was negative.
Suspecting a nasal polyp, an upper airway exam was performed during intubation prior to neuter the same day. The cat was sedated with a combination of intramuscular dexmedetomidine (2 mcg/kg), ketamine (5 mg/kg) and butorphanol (0.5 mg/kg). Using titrated propofol as an induction agent, intubation was attempted. No part of the larynx including the epiglottis was able to be visualized, the palate was noted to be abnormal and no polyp was identified. The cat was unable to be intubated despite multiple blind attempts. The neuter was performed under deep sedation routinely (no further sedation or inhalant use required) and the cat recovered uneventfully, though previously observed mild vestibular ataxia and left head tilt were more profound. Robenacoxib (2 mg/kg, SQ) was administered at the time of recovery. The cat was discharged with doxycycline 25 mg/5 mL oral suspension (5 mg/kg, PO, q 12 h), robenacoxib (3 mg/kg, PO, q 24 h) and continued ofloxacin (1 drop, OS, q 12 h).
In the immediate hours post-discharge, the owners noticed poor appetite, progressive stertor and vestibular ataxia. The cat was presented to an emergency service at aspecialty veterinary hospital for re-evaluation later in the evening. At presentation, vital parameters were within normal limits. The cat was quiet but alert and responsive with anisocoria (OS miotic, had a horizontal nystagmus with fast phase to the right, enophthalmic and elevated nictitans), a vestibular ataxia and left sided head tilt (Figure 1). Moderate inspiratory and expiratory stertor was appreciated; however, lung auscultation was unremarkable. The cat was given intravenous crystalloid fluids at 4 mL/h overnight, continued oral doxycycline (Cadila Healthcare Ltd.) (5 mg/kg, IV, q 12 h), maropitant (Zoetis) (1 mg/kg, IV, q24h) and oral gabapentin (Amneal Pharmaceuticals Pvt. Ltd.) (10 mg/kg, PO, q 8–12 h) for post-operative pain control. Blood glucose was mildly elevated the following morning during routine check (glucose 10.7 mmol/L [193 mg/dL]). The following day, a neurology consult was performed, and advanced imaging was recommended to rule out otitis media/interna prioritized over central causes for the vestibular disease. The owner declined imaging but approved an anesthetized oropharyngeal examination with videoscopy assistance.
Enlarge this image.FIGURE 1. The cat at initial presentation to the emergency service at a specialty veterinary hospital.
The cat was premedicated with butorphanol (Vetorphic, Vetone) (0.6 mg/kg IV) and glycopyrrolate (Glycopyrrolate, Xiromed, LLC) (0.01 mg/kg IV) with flow-by pre-oxygenation performed. Induction was performed with ketamine (Zetamine, Vetone)(5 mg/kg IV) followed by titrated propofol (Zoetis)(7.08 mg) to facilitate upper airway examination and intubation. Oxygenation was maintained during airway examination with neonatal oxygen prongs and oxygen flow at 1 L/min. Redundant tissue was noted in the nasopharyngeal region, and no epiglottis was visualized. Using endoscopic guidance (Karl Storz PN), the epiglottis was still not visualized. There was a blind ended space ventral to the arytenoid cartilages where the epiglottis would be presumed to originate (Figures 2 and 3). A small defect was appreciated on the proximal surface of the body of the tongue as well as two small divots at the mid to caudal aspect of the tongue, possibly prominent lingual tonsils (Figure 2). Intubation was achieved by first passing the small bronchoscope into the tracheal lumen and then guiding a polypropylene stylet past the arytenoids. A 3.0 mm endotracheal tube was passed over the stylet into the trachea (Figure 3). Retroflex of the scope further revealed nasopharyngeal stenosis to a degree limiting visualization (Figure 4). No abnormalities were visualized to explain Horner's syndrome. Computerized tomography (CT) (Toshiba Aquillon 64 slice; MXR Imaging) was recommended. The cat was moved to CT under the same anaesthetic episode. CT scan revealed bilaterally fluid-filled bullae and hyperostosis, regional asymmetric lymphadenomegaly, bilateral rhinitis (right worse than left side), absent epiglottis, thick soft palate and narrowed nasopharynx. There was no evidence of midline defect.
Enlarge this image.FIGURE 2. The tongue leading to larynx, no epiglottis visualized. Note tongue defect at proximal portion of image.
Enlarge this image.FIGURE 3. The space ventral to arytenoids is visualized where epiglottis should originate but appears to be absent.
The cat was stable throughout anaesthesia aside from mild hypotension, which was controlled with a dopamine (HIKMA Farmaceutica) constant rate infusion, 5 mcg/kg/min. Extubation was planned to be late in recovery, despite the cat desaturated soon after extubation with apparent cyanosis. The cat was given naloxone (Akorn, Inc.) reversal (10 mcg/kg IV) and atropine (Vetone) (0.02 mg/kg IV) once. Flow-by oxygen supplementation was continued as well as sedation with titrated propofol IV (Zoetis) (4 mg) to facilitate the placement of neonatal nasal oxygen prongs (Henry Schein Inc.). Oxygen was provided at 1L/min and tolerated well by the cat. Overnight, the cat remained eupneic with static stertor, pulse oximetry remained >96% and it ate normally. The cat was transitioned into an oxygen cage approximately 8 h after the placement of the nasal prongs with FiO2 at 40%–50%, and oxygen was weaned within the following 10 h. New medications added included dexamethasone SP (Bimeda-MTC Animal Health Inc.) (0.1 mg/kg IV q24h) and ampicillin/sulbactam (Meitheal Pharmaceuticals) (30 mg/kg IV q8h). The cat was discharged the following day with treatment for otitis interna with peripheral vestibular disease and concern for anatomic anomaly (nasopharyngeal stenosis and epiglottic aplasia) predisposing to chronic inflammatory upper airway disease. Primary goals were to monitor response to medical management at home with Clavamox (Zoetis) (13.75 mg/kg, PO, q12h) and prednisolone (Lloyd, Inc.) (0.5 mg/kg PO q24h).
The cat was rechecked 2 weeks later at the same specialty referral facility. There was improvement in neurologic status (resolved ataxia and miosis with remaining head tilt). The cat remained stertorous but seemed to be breathing well at home and was also eating normally. Re-check complete blood cell count through the reference lab revealed improvement in the neutrophilic leukocytosis (WBC 22.8 × 109/L (22.8 × 103/μL [RI 3.8 − 16.8 × 109/L])), neutrophils 13.4 × 109/L (13.4 × 103/μL [RI 1.9 − 9.5 × 109/L]) with new eosinophilia (4.7 × 109/L (4.7 × 103/μL [RI 0 − 1.52 × 109/L])) and thrombocytosis (503 × 109/L (503 × 103/μL [RI 165 – 494 × 109/L])). Conservative management was continued with prednisone, Clavamox dose adjusted for weight gain (increased to 0.5 mL PO q12 h), and fenbendazole (50 mg/kg PO q24h for 5 doses) was prescribed as part of routine deworming (due to new eosinophilia). Re-evaluation was recommended in 4 weeks. Later that same day, the cat had a syncopal episode while eating at home. The owners called the hospital and discussed the incident over the phone. The cat became rigid, fell over (some food fell from his mouth at this time), and it tried to get up and fell over again. The cat very quickly recovered and seemed normal. Emergency evaluation, thoracic radiographs, electrocardiogram and echocardiogram were discussed but declined since the cat seemed to spontaneously recover well. The next day, the cat was running and playing when suddenly it had another collapsing episode, but this time it did not recover and passed away at home. Necropsy was performed at a veterinary teaching hospital.
Postmortem findings revealed an elongated soft palate—the gingiva comprising the midline of the dorsal soft palate was diffusely dark red. Additionally, the epiglottis was not visible, and only a small portion of the arytenoid cartilages was visualized. After dissection of the oropharynx, the epiglottis was identified but entrapped by 2 cm of redundant, smooth, pink soft tissue (similar in appearance and texture to tissue of soft palate) extending from the root of the tongue to the larynx and partially obstructing the larynx (Figures 5 and 6) indicating that the initial diagnosis of epiglottic aplasia was incorrect. Once the tissue was reflected (Figure 6), the epiglottis appeared normal and fully formed. There was severe bilateral, chronic-active, suppurative otitis media and interna with numerous filamentous bacteria as well as cocci and bone remodelling affecting the tympanic bullae. The right side was more severely affected than the left side. Examination of the nasal cavity did not reveal any discharge, debris or other gross evidence of infection or inflammation. No damage to the ethmoid turbinates was appreciated. There was no comment on whether nasopharyngeal stenosis was observed in the report. A mild amount (3–5 mL) of serosanguinous fluid was present in the pericardial sac grossly, but no other cardiac or pulmonary abnormalities were reported in gross or histopathologic findings. Histologic examination of the nasal cavity, larynx, epiglottis and arytenoid/thyroid cartilages appeared normal.
Enlarge this image.FIGURE 5. Necropsy prior to dissection of tissue obscuring epiglottis (black arrow).
Enlarge this image.FIGURE 6. Necropsy post-dissection of obstructive tissue revealing the fully formed epiglottis (black arrow).
This report describes a case of epiglottic entrapment in a cat resulting in presumed upper airway obstruction. The cat was also diagnosed with severe otitis media/interna as well as nasopharyngeal stenosis. It is unclear whether these anatomical anomalies predisposed the cat to development of otitis (possibly due to obstruction of eustachian tube). There are several disorders of the epiglottis described in veterinary medicine. Forms of epiglottic entrapment have been reported in horses, and there is one case in dogs (Boles et al., 1978; Phillips, 2022). These examples have many similarities but are not completely consistent with the findings in the cat described above.
Epiglottic entrapment was first reported in horses in 1978 (Boles et al., 1978). The aryepiglottic folds completely cover the apex and lateral margins of the epiglottis. The epiglottis remains in its appropriate position (ventral to the soft palate) and the general shape of the epiglottis is visible on examination; however, the normal vascular pattern and notched edge of the epiglottis cannot be seen. The most commonly reported clinical signs are loud respiratory noise and exercise intolerance. Less commonly, coughing, nasal discharge and head shaking are reported. Treatment is surgical transection of the aryepiglottic fold laryngeal abnormality. A congenital predisposition was suggested since a large number of animals diagnosed with this condition were young (less than or equal to 2 years old). Based on the findings described in post-mortem examination, the cat in this case summary was similar to this condition; however, the cat's epiglottis was described to be obscured by redundant soft tissue rather than true aryepiglottic folds as in equine epiglottic entrapment.
In dogs, there is one case report of a similar abnormality in a 22-month-old English Bulldog (Bedford, 1983). Laryngoscopic exam in this dog revealed diffuse, severe oedema and static displacement of redundant glossoepiglottic mucosa causing complete obstruction of the larynx and epiglottic entrapment. The dog was dyspneic due to upper airway obstruction but had no stertor at rest prior to dyspneic event. In addition to routine brachycephalic obstructive airway surgery, the redundant mucosa was surgically excised, and a temporary tracheostomy tube was utilized to facilitate safe recovery. Histopathology of the mucosa noted mild, chronic, suppurative and lymphoplasmacytic laryngitis with marked oedema and fibroplasia. The dog did well with the procedure and demonstrated healing at the post-operative recheck. Another report in Thoroughbred horses describes transient displacement of the glossoepiglottic mucosa obstructing the airway during inspiration in patients with chronic airway disease. The aetiology was considered secondary to chronic increased inspiratory effort (vs. congenital as is the suspicion in this case). This was treated similarly with surgical resection (Bedford, 1983).
A similar condition that is rarely reported in dogs is termed epiglottic retroversion. This is characterized by the obstruction of the rima glottis by the epiglottis via spontaneous retroflexion that occurs during inspiration (Phillips, 2022). Postulated causes of epiglottis retroversion include hypothyroidism-related neuropathy and denervation of the hypoglossal and/or glossopharyngeal nerves, epiglottic trauma such as fracture and malacia. In reported cases, dogs were older than 5 years. Clinical signs included severe inspiratory stridor and dyspnea. Current methods for surgical correction include subtotal epiglottectomy, temporary or permanent epiglottopexy or combination of both (Ambrosio & Brigger, 2012; Skerrett et al., 2015).
In paediatric medicine, laryngomalacia is described as the most common congenital laryngeal abnormality in neonates (Bedwell & Zalzal, 2016; Flanders & Thompson, 2009). Anatomic abnormalities described in laryngomalacia include elongated, redundant or shortened aryepiglottic folds, retropositioned epiglottis and prolapsed arytenoid mucosa. Although the exact cause of laryngomalacia is unknown, aetiologies that have been described include poor rigidity of the laryngeal cartilages, laryngeal inflammation secondary to gastroesophageal reflux and defective neuromuscular control of the larynx. Affected patients often exhibit inspiratory stridor and respiratory distress. Although this can be conservatively managed and may self-resolve by 12–24 months of age, some patients require surgical treatment for persistent dyspnea, difficulty feeding or failure to thrive. Severely affected patients can develop cardiopulmonary sequelae including pulmonary hypertension, cor pulmonale and pectus excavatum. The standard surgery of choice is supraglottoplasty which is surgical correction of any anatomic abnormalities using microlaryngeal instrumentation. Newer techniques using radiofrequency ablation (modified microscopic radiofrequency ablation supraglottoplasty) have also been described to have better efficacy (Garritano & Carr, 2014).
In this case, an initial clinical diagnosis was made of epiglottic aplasia, of which no reports exist in felines. In people, it is a rare condition and thought to be a genetic anomaly. The necropsy allowed further exploration and identified epiglottic entrapment due to redundant tissue at the base of the tongue obscuring the epiglottis. The tissue had an appearance similar to the normal tissue of the soft palate, and thus the diagnosis of severely elongated soft palate is reported. Histopathology of the tissue was not performed.
The primary imaging modality utilized was bronchoscopy to facilitate intubation followed immediately by CT. In retrospect, fluoroscopy and contrast swallow study may have allowed further characterization of anatomic abnormalities pre-mortem. MRI may have also been utilized over CT to better differentiate soft tissues, cartilaginous structures and muscle of the upper airway in this cat.
Based on the collective information obtained from the endoscopic examination of the nasopharynx and CT scan, it is plausible that chronic negative pressure from nasopharyngeal stenosis contributed to airway abnormalities in this cat. Nasopharyngeal stenosis was not a finding in necropsy; however, antemortem, this was suspected to be a major contributor to the cat's clinical signs.
Nasopharyngeal stenosis is an uncommonly reported condition in cats that is often attributed to scar tissue formation secondary to chronic upper respiratory infections. Clinical signs can include stertorous breathing, sneezing and oculonasal discharge (Kuehn, 2006; Pu et al., 2018). Balloon dilation is one treatment option that has been proposed to help alleviate this condition and involves using an esophageal dilation balloon catheter to attempt dilation of the narrowed tissue within the nasopharynx. The benefit of the procedure is that it is minimally invasive and relatively easy to perform; however, relief is generally temporary for the patient with one study showing clinical sign recurrence within weeks to months for most cats (Henderson et al., 2004). Balloon dilation, although challenging in a patient of this size, may have been a consideration as the treatment for this cat if further evidence of nasopharyngeal stenosis was identified.
CONCLUSIONSTo the authors’ knowledge, this is the first report of these oropharyngeal anatomic abnormalities in a cat.
AUTHOR CONTRIBUTIONSConceptualization, investigation, writing—original draft and writing—review and editing: Diana Victoria Arbona. Conceptualization, investigation, supervision, writing—original draft and writing—review and editing: Chap Pratt. Conceptualization, investigation, supervision, writing—original draft and writing—review and editing: Caitlin Tearney. Supervision and writing—review and editing: Stephanie Istvan.
ACKNOWLEDGEMENTSThe authors would like to thank the Veterinary Diagnostic Laboratory at Colorado State University and Doctors Eileen Larsen, DVM and Allison Vilander, DVM, PhD, DACVP for their contribution to the findings in this report.
FUNDING INFORMATIONNo sources of support in the form of grants, equipment, or drugs were provided for the preparation of this manuscript.
CONFLICT OF INTEREST STATEMENTThe authors declare no conflict of interest.
DATA AVAILABILITY STATEMENTno data.
PEER REVIEWThe peer review history for this article is available at
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; Pratt, Chap 2 ; Tearney, Caitlin 3 ; Istvan, Stephanie 1 1 Veterinary Specialty Hospital – Sorrento Valley, San Diego, California, USA
2 Colorado Animal Specialty and Emergency, Critical Care, Boulder, Colorado, USA
3 Veterinary Medical Center: Anesthesia, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota, USA