Recent studies have reported that nasal turbinate and thickening of the soft tissues in the nasopharynx may be the primary anatomic component of BOAS [3-6]. When the turbinate bone exists beyond normal anatomical limits because of a structural deformity, it is called an aberrant turbinate. A caudal aberrant turbinate is a caudal extension of the maxilla, part of the nasopharynx into the nasopharyngeal meatus, or both [6,7].

The etiology mechanism of the generation of aberrant turbinate is not entirely understood. Several factors are believed to contribute to the formation of the aberrant turbinate. Selective breeding within the brachycephaly results in shortened facial bones and dorsorotation of the teeth, leading to the displacement of the nasal structures [6]. The mechanism does not appear to be operative in brachycephalic breeds, in which the growth of normal nasal conchae stops before the mucosal layers of adjacent turbinate lamellae come into contact with each other [8].

This report describes the radiography and computed tomography (CT) features of a caudal aberrant turbinate in a dog with BOAS.

A 5-year-old spayed female Pug presented with left ear discharge and respiratory distress. The patient had a history of left otitis media and interna diagnosed 1 year ago. The dog was treated with prednisolone, amoxicillin, and clavulanic acid.

Skull radiography showed increased opacity and calcification of bilateral ear canals, a thick and elongated soft palate, and a narrow nasopharynx, suggesting BOAS (Fig. 1). Thoracic radiography revealed mild increased lung opacity attributed to obesity. Subsequently, skull CT (Alexion; Canon Medical Systems, Japan) and brain magnetic resonance imaging (MRI) (1.5 Tesla unit, Vantage Elan; Canon Medical Systems) were performed to evaluate the middle and inner ear structures. The patient was positioned in sternal recumbency under general anesthesia. Anesthesia was premedicated with midazolam at a dose of 0.2 mg/kg, induced with propofol at a dose of 4 mg/kg intravenously and maintained with isoflurane in oxygen. The CT parameters were a 120 kilovoltage peak, 150 milliampere-seconds, 2.0 mm slice thickness, 2.0 mm interval, 0.75 second rotation time, and 0.938 collimation beam pitch. Post-contrast CT images were acquired at 7, 30 and 90 seconds after injecting 600 mg iodine/kg iohexol (Omnipaque; GE Healthcard, Ireland) intravenously. The sagittal and dorsal reconstruction images in the soft tissue window and bone window were acquired. The caudal margin of the soft palate extended to the posterior of the cricoid cartilage and was 8.5 mm in thickness and 7.2 cm in length. The nasopharynx was very narrow owing to this thickened soft palate (Fig. 2A and B). The turbinate structures were observed medial to the bilateral nasal glands, extending caudally from the level of the ventral nasal meatus. This was longer on the left side, extending to the level of the nasopharynx caudal to the vomer (Fig. 2C-F). This was believed to be a caudal aberrant turbinate, given that the patient is a brachycephalic breed. The wall thickness of the bilateral external ear canal was thick, and calcification foci were observed. The left proximal external acoustic meatus and tympanic bulla were filled with soft tissue-dense material. In addition, a small amount of the same material was present inside the right tympanic cavity. The left tympanic bulla wall was thinner than the right, with some evidence of bone lysis (Fig. 2E). A brain MRI showed that the left inner ear vestibule and cochlea lost T2 hyperintensity. The unambiguous diagnosis was BOAS, bilateral otitis externa, media (severe on the left side, mild on the right side), and left otitis interna.

Twenty-six days later, the patient presented with severe respiratory distress. The radiographic findings showed increased lung opacity of the caudodorsal lung field and severe gastric dilation secondary to aerophagia. These led to a tentative diagnosis of non-cardiogenic pulmonary edema secondary to chronic airway obstruction.

The patient was treated with butorphanol, inhaled corticosteroid (fluticasone with salmeterol), and oxygen therapy. Two days later, thoracic radiography revealed decreased lung opacity. Surgical intervention was performed as folded flap palatoplasty and left total ear canal ablation. Despite treatment, the dog expired due to persistent respiratory distress, and necropsy was not performed.

The nose has the greatest source of flow resistance of the airway system, accounting for approximately 76.5%, which is particularly pronounced in carnivores [9,10]. Intranasal resistance was reported to be significantly higher in brachycephalic breeds because shorter skulls have shorter nasopharyngeal pathways [11]. Pugs are a breed characterized by shorter facial bones than other brachycephalic breeds, with several abnormal intranasal structures [6]. One of these is the caudal aberrant turbinate, which extends into the nasopharynx, and was reported to occur in one study as 12 out of 30 Pugs and 3 out of 30 French Bulldogs [12], and in another study as 9 out of 17 Pugs and at a higher frequency compared to other brachycephalic breeds [5].

The caudal aberrant turbinate are classified in a 5-point ordinal grading scheme depending on the degree of caudal extension of turbinate: grade 0 (normal), there are no turbinate visible in the ventral nasal meatus; grade 1 (minimal), the turbinate bone is observed inside the ventral nasal meatus; grade 2 (mild), turbinate bone is inside the nasopharyngeal meatus; grade 3, (moderate) turbinate bone is inside the choanae; grade 4 (severe), turbinate bone is when the turbinate extends into the interior of the nasopharynx [13].

The debate over how much caudal aberrant turbinate impacts clinical symptoms continues. A previous study reported that severe caudal aberrant turbinate is relatively common (21%) in dogs with clinical signs of brachycephaly [5], which may contribute to a respiratory tract obstruction by occupying the normally open-air passages with excessive soft tissue [14]. In addition, a report suggests that the mucosal layers of turbinate in the brachycephalic nasal airway make multiple contacts, interfere with normal air transfer function, and contribute to obstruction. Nevertheless, a recent study showed that the narrowest nasopharyngeal cross-sectional areas were located dorsal to the caudal end of the soft palate, even in dogs with severe caudal aberrant turbinate [12]. Furthermore, in 40 clinically healthy English Bulldogs, caudal aberrant turbinate was identified with a 100% probability of grade 1 to 3 [13]. Suggesting that the impact of an aberrant turbinate on respiratory obstruction is unclear.

The choice of imaging modalities for diagnosing BOAS and identifying caudal aberrant turbinate deserves discussion. Currently, a diagnosis of BOAS is based mostly on the clinical signs, radiography, endoscopy, or fluoroscopy. Radiography can evaluate the soft palate, but an evaluation of the intranasal bony structures is difficult because of the complexity of the cranial structures. An examination to evaluate the nasopharynx is indicated because caudal aberrant turbinate is common in brachycephalic dogs suffering from BOAS, especially grade 4, which was reported to be approximately 40% in Pugs and 10% in French Bulldogs [15]. A complementary method is rhinoscopy, but it has the potential for difficult visualization because of nasal discharge and hemorrhage. CT bone window imaging allows for a detailed assessment, including delicate nasal structures, the degree of various abnormalities such as vestibular stenosis and malformation of the conchae. Therefore, CT imaging is strongly recommended if anesthesia is available in a brachycephalic dog.

In addition, middle ear effusion is commonly observed as an incidental finding in brachycephaly, up to 41% in one study [16]. A dysfunction of the Eustachian tube is presumed to be a major cause [17], and other factors such as small tympanic bullae volume, tortuous ear canal, and thick soft palate are believed to be multifactorial [15,18]. On the other hand, previous studies in brachycephalic breeds may underestimate the problem related to otitis media because the CT and MRI findings of otitis media other than internal effusion have not been evaluated in previous studies. Therefore, the above factors can be considered as a cause if fluid in the middle ear is observed in brachycephalic breeds, and the possibility of otitis media should be considered [16].

In BOAS patients, especially in Pugs, in addition to typical anatomical anomalies such as nasal stenosis or elongated soft palate, the intranasal structural problems are likely to be present, and caudal aberrant turbinate is common. This should be considered one of the potential reasons for BOAS. A further evaluation of various nasal anomalies is possible with CT, and CT images in the bone window of the skull are recommended for a meticulous evaluation of the nasal structures if anesthesia is feasible in brachycephalic breeds. Nevertheless, the association between the caudal aberrant turbinate and clinical symptoms remains unclear and warrants further study.