Introduction
A 3-year-old 17.5-kg (38.5-lb) spayed female mixed-breed (Labrador Retriever cross) dog was presented to the University of Wisconsin Veterinary Care Small Animal Internal Medicine service because of a 9-month history of bilateral mucopurulent nasal discharge, sneezing, and signs of nasal congestion that were reported to have started after a routine ovariohysterectomy.
Prior to referral, the dog had been evaluated at a primary care practice and at another tertiary care facility. On physical examination, bilaterally decreased nasal airflow and upper respiratory stertor were noted. Clinicopathologic findings (results of a CBC, serum biochemical analysis, and urinalysis) were within respective reference ranges except for neutrophilic leukocytosis (19.5 × 103 WBCs/µL [reference range, 6.0 × 103 to 17.0 × 103 WBCs/µL] with 15.6 × 103 segmented neutrophils/µL [reference range, 3.0 × 103 to 11.5 × 103 segmented neutrophils/µL]). Thoracic radiography revealed a mild diffuse bronchial pattern and normal to minimally tortuous pulmonary vasculature in the periphery, consistent with the dog's history of previously diagnosed and treated heartworm disease. The dog underwent general anesthesia for CT of the skull and rhinoscopy. The CT findings included severe NPS, suspected regional reactive lymphadenopathy, and bilateral nondestructive rhinitis with associated periostitis and secondary sinusitis. Retrograde rhinoscopy confirmed severe, nearly complete membranous NPS with mucopurulent nasal discharge. Antegrade rhinoscopy revealed increased nasal discharge and apparently normal nasal turbinates. Medical management approaches prior to tertiary referral included antimicrobials (doxycycline [dosage and duration unspecified], amoxicillin–clavulanic acid [15.2 mg/kg {6.91 mg/lb}, PO, q 12 h] for 28 days, and enrofloxacin [8.2 mg/kg {3.73 mg/lb}, PO, q 24 h] for 14 days), prednisone (0.6 mg/kg [0.27 mg/lb], PO, q 24 h for 5 weeks), carprofen (2.3 mg/kg [1.05 mg/lb], PO, q 12 h), chlorpheniramine (0.24 mg/kg [0.11 mg/lb], PO, q 12 h), and periodic nasal flushes under general anesthesia. None of the treatments provided long-lasting resolution of the dog's clinical signs.
At the time of evaluation at University of Wisconsin Veterinary Care, the dog's owner reported copious bilateral mucopurulent nasal discharge and continuous stertorous breathing with intermittent open-mouthed breathing (including episodes that interrupted the dog's sleep). The dog was mildly lethargic and reluctant to exercise. On physical examination, intermittent sneezing with thick green bilateral mucopurulent nasal discharge was noted. Airflow was absent from the right naris and markedly reduced from the left naris. Stertor was obvious when the dog was at rest. There were bilaterally increased bronchovesicular sounds on thoracic auscultation, and increased inspiratory effort was evident while the dog was sleeping. Results of serum biochemical analysis were within respective reference ranges.
Retrospective review of the previously obtained CT images of the skull by a board-certified veterinary radiologist revealed severe bilateral osseous narrowing of the choanal region, which measured 2 mm dorsoventrally at its narrowest point; severe circumferential thickening and sclerosis of the palatine bone surrounding the choanae; and dorsal bowing of the caudalmost aspect of the hard palate (Figure 1). These findings were consistent with severe bilateral partial osseous choanal atresia in addition to the previously diagnosed NPS. Bilateral congenital frontal sinus hypoplasia was also noted, with osseous malformation or reactive periostitis of the frontal bone secondary to chronic frontal sinusitis.
Treatment options discussed with the owner included surgical debridement (ventral rhinotomy) with covered nasopharyngeal stent placement, balloon dilation of the region affected by membranous NPS,1,2 permanent tracheostomy,3 or medical management. Surgical debridement (ventral rhinotomy) with subsequent placement of a covered nasopharyngeal stent was recommended and elected. A covered self-expandable nasopharyngeal stent was chosen on the basis of a previous report2 that described an improved success rate (compared with that for balloon dilation alone) and reduced risk of tissue ingrowth (compared with use of an uncovered nasopharyngeal stent). Surgical goals included debridement and enlargement of the bony stenosis, opening and reconstruction of the membranous stenosis, and placement of the stent to span both the bony and membranous areas. Presurgical planning included use of the previously obtained CT images to determine an appropriate stent length for this purpose (Figure 2).
In the interim, azithromycin (7.1 mg/kg [3.23 mg/lb], PO, q 24 h for 5 days and then q 48 h for 15 days), prednisone (1.1 mg/kg [0.5 mg/lb], PO, q 24 h tapered over 20 days), ondansetron (0.5 mg/kg [0.23 mg/lb], PO, q 12 h for 3 days), nebulization with water (q 12 h), and saline solution drops (over-the-counter pediatric preparation; 2 drops/naris, q 12 h) were prescribed. With this medical treatment, a notable improvement in the dog's clinical signs was reported but diminished as the prednisone dosage was tapered to 0.3 mg/kg (0.14 mg/lb), PO, every 24 hours.
Ten weeks after the initial referral evaluation, the dog was returned to University of Wisconsin Veterinary Care for surgical treatment of choanal atresia and NPS. Results of clinicopathologic testing, including a CBC, serum biochemical analysis, and coagulation times, were within respective reference ranges. Presurgical retrograde rhinoscopy confirmed the presence of severe membranous NPS, with 1 small communication to the nasal passages observed (Figure 3). Red rubber catheters (ranging from 5F to 12F in diameter) could not be passed antegrade through the nares.
Anesthesia was induced with propofol (1.18 mg/kg [0.54 mg/lb], IV) and maintained with sevoflurane in oxygen. Cefazolin sodium (22 mg/kg [10 mg/lb], IV, q 60 min) was administered intraoperatively. The dog was placed in dorsal recumbency, and a transpalatal ventral rhinotomy was performed. A midline incision was made through the palatine tissue overlying the caudal third of the hard palate and rostral half of the soft palate, as previously described.3 The tissue overlying the caudal aspect of the hard palate was elevated from midline, and a burr was used to remove approximately 10 mm of bone from the caudal edge of the hard palate to the level of the alveolar process of the maxilla. The nasopharynx was entered, and the soft tissue and bone of the vomerine crest and groove were debrided with a pneumatic burr.
Following bony debridement, communication between the pharynx, nasopharynx, and nasal passages was established by incising the stenotic mucosa with a No. 15 scalpel blade (Figure 4). The oropharyngeal mucosa was sutured to the adjacent edges of the nasopharyngeal mucosa with 4-0 polyglyconate suture in a simple interrupted pattern to establish a nasopharyngeal opening approximately 12 mm in diameter. An 8F red rubber catheter was passed antegrade from each naris into the pharynx to confirm complete patency of the nasopharyngeal area.
A 0.035-inch hydrophilic angle-tipped guidewire was placed antegrade through the left naris into the pharynx. A covered self-expandable nasopharyngeal stenta (12 × 40 mm) was placed over the wire, passed retrograde into the nasopharynx, and deployed with fluoroscopic guidance and direct visual monitoring. The stent position was easily adjusted through the surgically created opening with forceps. A single horizontal mattress suture (2-0 polypropylene) was used to secure the stent to the soft palate. Owing to the length of the area of bony debridement and the caudal extent of the reconstruction of the nasopharynx and oropharynx, the stent did not completely span the newly formed nasopharyngeal passage. An approximately 10-mm-long gap was present between the caudal aspect of the palatine bone and the rostral end of the stent (Figure 4). The dorsal (nasopharyngeal) mucosa of the soft palate was closed with 4-0 polyglyconate suture in a simple continuous pattern. The ventral (oropharyngeal) mucosa was closed in 2 layers with a 4-0 polyglyconate suture in a simple interrupted pattern followed by a simple continuous pattern. Postoperative radiography of the skull confirmed stent placement in the rostral portion of the nasopharynx spanning the previous region of NPS (Figure 5).
The dog recovered uneventfully and was treated overnight with isotonic crystalloid fluids (53 mL/kg/d [24.1 mL/lb/d]), dexamethasone sodium phosphate (0.07 mg/kg [0.03 mg/lb], IV, q 24 h), and fentanyl (3 to 6 µg/kg/h [1.36 to 2.72 µg/lb/h], by continuous rate IV infusion). The following day, the dog had no appreciable nasal discharge and was breathing through the nares with minimal stertor. The dog was discharged approximately 60 hours after surgery. The owner was instructed to administer acetaminophen (13.9 mg/kg [6.32 mg/lb], PO, q 8 h for 5 days), amoxicillin–clavulanic acid (13.9 mg/kg, PO, q 12 h for 14 days), and prednisone (0.3 mg/kg, PO, q 12 h for 14 days) and to feed soft food only until recheck examination (14 days after treatment).
After discharge from the hospital, the dog was initially reported to be free of signs; however, nasopharyngeal signs including stertor and mucopurulent discharge progressively returned and gagging developed after abrupt discontinuation of prednisone 2 weeks after surgery. Three weeks after surgery, the dog was reevaluated. A wet cough and pronounced stertor were identified during physical examination. Oral examination revealed that the incision site in the palate was healing well. Radiography of the skull revealed no evidence of stent migration or fracture. Retrograde rhinoscopy with the dog under general anesthesia revealed marked mucopurulent discharge occluding the lumen of the stent. Following antegrade nasal flushing, the entire length of the stent was determined to be patent; however, a soft tissue stricture occluding > 80% of the lumen opening was detected immediately rostral to the stent (Figure 6). A 14F red rubber catheter was passed antegrade through the stricture with minimal resistance. The dog recovered from anesthesia uneventfully and was discharged from the hospital with prednisone (0.4 mg/kg [0.18 mg/lb], PO, q 12 h for 5 days, followed by 0.2 mg/kg [0.09 mg/lb], PO, q 12 h until reevaluation).
One week later, the dog underwent a second procedure to address the stricture rostral to the stent. After nasal flushing, nasopharyngeal balloon dilation of the stricture was performed as previously described1,2 with a percutaneous transluminal angioplasty balloonb (10 × 40 mm). A second covered self-expandable nasopharyngeal stenta (12 × 40 mm) was placed in a retrograde manner over the same guidewire used for balloon dilation, and the stent was deployed with fluoroscopic guidance. The deployed second stent spanned the complete length of the stricture with approximately 75% overlap within the original stent. Retrograde rhinoscopy confirmed patency of both stents. The new stent was secured to the soft palate with 2 toggle sutures.c Postoperative skull radiographs confirmed correct positioning of both stents within the caudal aspect of the nasal cavity and rostral portion of the nasopharynx.
The dog recovered uneventfully and was managed overnight with administration of isotonic crystalloid fluids (29 mL/kg/d [13.2 mL/lb/d]), dexamethasone sodium phosphate (0.12 mg/kg [0.05 mg/lb], IV, once), ketamine (3 to 6 µg/kg/min, by continuous rate IV infusion), and 0.5% proparacaine hydrochloride solution (2 drops in each naris as needed to reduce epistaxis and sneezing). The next day, stertor and nasal discharge had largely resolved. The dog was discharged from the hospital 24 hours after stent placement. The owner was instructed to administer prednisone (0.6 mg/kg, PO, q 24 h, tapered slowly over 3 months), azithromycin (7.6 mg/kg [3.45 mg/lb], PO, q 24 h for 5 days and then q 48 h for 30 days), and saline solution drops (2 drops/naris, q 12 h, chronically). The nasal drops were discontinued after 3 days because of the dog's noncompliance.
The dog had no recurrence of severe nasal signs and no clinical signs associated with nasopharyngeal stent placement or soft palate surgery (eg, signs of oral discomfort or dysphagia). Three months after stent placement, the prednisone treatment was replaced with fluticasone (220 µg, inhalation via facemask, q 12 h). Long-term steroid administration was prescribed because of the potential to prevent chronic rhinosinusitis4,5 and granulation tissue formation. At a recheck examination 13 weeks after stent placement (1 week after prednisone treatment was discontinued), physical examination variables were deemed normal and stable stent position was confirmed with skull radiography (Figure 7). The owner reported that the dog had complete resolution of all nasal discharge and sneezing and had normal respiratory effort with no recurrence of gagging episodes. There was marked improvement in stertor, with only a brief snorting noise noted once or twice per day. Four months after the placement of the second stent, the dog was reported to have increased stertor (described as reverberation) during deep sleep. This resolved after treatment with azithromycin (13.7 mg/kg [6.23 mg/lb], PO, q 24 h for 5 days and then q 48 h for 10 days). Eleven months after placement of the second nasopharyngeal stent, the dog had no progression in clinical signs. Elective stent removal was considered but was ultimately not performed because the dog's tolerance of the implants was considered excellent, and there was concern about a possible relapse of NPS if these were removed.
Discussion
To the authors’ knowledge, this report provided the first description of bilateral partial osseous choanal atresia and NPS in a dog and its successful management with a combination of surgical and minimally invasive stenting techniques. Choanal atresia is a rare congenital anomaly of dogs in which there is incomplete canalization of the choanae (the oval openings of the nasopharyngeal meatuses) into the nasopharynx.3,6 This causes partial or complete obstruction of airflow between the choanae and nasopharynx, resulting in sneezing, nasal discharge, stertor, and open-mouthed breathing.3,6 Choanal atresia is classified on the basis of position (unilateral or bilateral), severity (partial or complete), and tissue type (osseous or membranous).6 To the author's knowledge, previously reported cases in dogs were reported only for Shih Tzus3,6 and have not been associated with concurrent congenital defects (eg, coloboma, heart defects, growth anomalies, or genitourinary defects) that have been described for children with choanal atresia.7
The dog of the present report had bilateral partial osseous choanal atresia with concurrent acquired NPS, and we are unaware of any reports of this form of choanal atresia in dogs. Advanced imaging techniques revealed multiple abnormalities consistent with those found in children with choanal atresia, including narrowing of the caudal aspect of the choanae, thickening of the vomer bone, and dorsal bowing of the hard palate.8 Acquired NPS due to aspiration rhinitis and nasopharyngeal irritation secondary to a regurgitation episode was suspected owing to the location of the stenosis (in the rostral third of the nasopharynx)2 and the close association between timing of ovariohysterectomy and reported onset of clinical signs.2,9 Alternatively, the soft tissue stenosis may have represented a form of membranous choanal atresia not yet described in the veterinary literature.
A literature search revealed 2 reports2,3 of attempted treatment of choanal atresia in dogs. In 1 dog, bilateral partial membranous choanal atresia was diagnosed.3 Correction was attempted with ventral rhinotomy, and clinical signs resolved for 2 weeks before open-mouthed breathing and stertor recurred. An endoscopic examination 4 weeks after surgery revealed stricture formation at the rhinotomy site, and the dog underwent permanent tracheostomy as a salvage procedure. Eight months later, the dog was reportedly doing well with a good quality of life, but normal nasal airflow was not reestablished. The other dog was included in a case series2 of dogs and cats affected by benign nasopharyngeal stenoses. In that dog, membranous choanal atresia (described as suspected congenital webbing) was diagnosed. Complications and outcome for this dog were not explicitly reported; however, the general success rate of balloon dilation followed by the placement of covered or uncovered nasopharyngeal stents was found to be significantly reduced in cases that involved imperforate membranes.2
For the dog of the present report, a combination of surgical debridement of the osseous malformation and stenting of the reconstructed nasopharyngeal area was considered the most viable option. In similar cases in children, a variety of alternatives including transnasal endoscopic and laser procedures are available.7 These procedures were not considered as options because of a lack of specialized equipment and expertise.
Success in preventing postoperative stenosis3 11 months after the second surgery in this dog was considered attributable to the use of a covered nasopharyngeal stent. In children undergoing endoscopic or surgical correction of choanal atresia, the use of postprocedural stenting is controversial, with multiple studies10–13 finding no impact of stenting on complication rates or outcome. However, available evidence in the management of acquired NPS in dogs appears to support the use of temporary or permanent stents in all dogs undergoing nasopharyngeal interventions.2 The benefit of stenting in dogs with NPS may be related to the underlying pathological process, a species-specific tendency for dogs to form strictures after corrective surgery in this region, or lack of minimally traumatic treatment options.
An important cause of morbidity in the dog of the present report was inadequate stent length during the first procedure, resulting in postoperative stricture formation and the need for a revision procedure. The reason for the miscalculated stent length was attributed to underestimation of the extent of bony debridement that was necessary to fully open the nasopharynx, as well as the caudal extent of the reconstruction when correcting the membranous NPS. In retrospect, it might have been beneficial to place the stent as far rostrally as possible to span the area of the more extensive bony debridement instead of the more caudal region. Fortunately, the stricture that developed rostral to the first stent was well managed with an identically sized stent deployed to overlap with the original stent and span the affected area. This technique has previously been reported to be successful in similar applications.1 Predetermined estimation of the extent of planned surgical debridement (on the basis of CT measurements) or intraoperative stent sizing would likely avoid this complication in other dogs.
Importantly, the approach used for the dog of this report provided a viable alternative to permanent tracheostomy, which is a salvage procedure described for dogs severely affected with choanal atresia. The results for this patient suggested that ventral rhinotomy and covered nasopharyngeal stent placement can be used successfully for the management of osseous choanal atresia in dogs.
Footnotes
Vet Stent-Nasopharyngeal, Infiniti Medical LLC, Redwood City, Calif.
Tyshak I, Infiniti Medical LLC, Redwood City, Calif.
T-toggle, Infiniti Medical LLC, Redwood City, Calif.
Abbreviations
NPS | Nasopharyngeal stenosis |
Acknowledgments
The authors declare that there were no conflicts of interest.
The authors thank Drs. Jeffrey Solomon and Sarit Dhupa for technical assistance with presurgical planning.
References
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