34th Annual Scientific Meeting proceedings

Traditional multilevel surgery (MLS), addressing stenotic nares, elongated soft palate, and resection of everted sacculi alone, produces variable results and does not seem to alleviate upper airway obstruction enough [1, 2]. Nasal airway resistance is almost ten times higher in brachycephalic breeds [3]. Intranasal obstruction is diagnosed by the presence and amount of mucosal contact points (MCPs). Dogs[72][35][73][72][72] depend on the cooling effect of evaporation of fluids on mucous membranes to regulate their body temperature. Partial or complete obliteration of nasal passageways hinders and changes nasal airflow[74, 75][25, 76][22, 25][74, 77][22]. MCPs are are thought to origin from rostral and caudal aberrant turbinates (RATs and CATs) [4, 5]. s which branch off the ventral turbinate or the ethmoturbinates and expand into the nasal meati, the choanae or beyond  We assume that small patient number may have contributed to the lack of significance in these patients.In our experience, and referring to the visual examples of CATs available in the literature, CATs and RATs are not rarely hypertrophied and do contribute to the formation ofnot contribute to  MCPs only by being touched by enlarged nasal turbinates or maxilloturbinates [6, 7].  We side with the interpretation by Liu et al that these rostrally and caudally extending branches serve as a compensatory mechanism for the restricted intranasal space in brachycephalic dogs, without contributing to intranasal obstruction [1]. MCPs, so far, have been treated by turbinectomy, but the effect of turbinectomy on nasal airflow, cooling efficiency, and a histological examination of the rapidly regrowing intranasal structures have not been carried out in dogs [4, 8-12]. The efficacy of canine body temperature regulation depends on nasal anatomy, mucosal surface area and flow dynamics. Most heat exchange takes place on the mucosa of the branches of the maxilloturbinate. Partial or complete obliteration caused by MCPs changes nasal airflow and reduces the contact between air and mucosa, theoretically reducing the ability to exercise, and prolonging recovery time [13-16]. Computational fluid dynamics (CFD) have shown a reduction of mucosal interaction after turbinectomy in humans and even partial turbinectomy leads to an increased velocity and laminar flow in the areas of resection while the interaction with the remaining mucosal surfaces decreases [17, 18]. Subjective satisfaction after turbinectomy in humans is low and turbinoplasty is often chosen over turbinectomy [19-23]. These findings should be considered when treatment for hypertrophic turbinals in dogs with BOAS is considered.

Radiofrequency Volumetric Tissue Reduction (RFTVR) is n a turbinoplasty procedure that has proven to be effective and minimal invasive. RFVTR in people is routinely used performed under local without general anaesthesia and as an outpatient procedure [20, 24-26]. For the treatment of hypertrophic turbinates, a bipolar radiofrequency probe is inserted in the lamina propria between the mucous membrane and the bone. Radiofrequency Ablation is a subset of radiofrequency surgery, designed to be applied inside the tissue with a temperature range between 40-65°C [27, 28]. At this temperature range, protein is denaturated and heat conduction to deeper tissue layers is minimal. In RFVTR a bipolar RFA probe is inserted into the lamina propria of the turbinate and the venous plexus is partially destroyed locally, while the mucous membrane over the defect remains intact and functional. After a healing period the defect is closed and the volume of the turbinate is reduced [19, 29-33]. With the tissue in direct contact to the bipolar electrode only a very small area of tissue adjacent to the probe is denaturated. Inside the probe the electrons serve as charger carriers while inside the tissue the cell membrane ions (Na⁺, N⁺, Cl⁺) carry the current. The current activates movement of the ions and heat is generated due to friction. Radiofrequency units work with a temperature range between 40-70°C. In this range denaturation of the proteins occurs, but neither cell wall rupture (100°C), nor carbonization (250°C) This creates a well-controlled, circumscribed lesion in the deeper layers of the turbinates [39, 40, 44, 45]. This explains why the ciliary lining of the treated turbinates remains and mucociliary clearing of the treated turbinates is not altered [53, 57]. With fewer turbinates turbulent flow is partially to completely replaced by laminar flow causing further decrease in the contact between air and mucous membranes [30]. Human patients with empty nose syndrome even tend to feel dyspnea despite reduced airway resistance [25]. It is unknown if hypertrophic turbinates in humans share common histological characteristics with hypertrophic turbinates in BOAS. In humans engorgement of the erectile tissue in the inferior turbinate is one of the main pathophysiological factors, which has not been described for dogs [28, 44, 45, 74]. Our data shows that it is time to reconsider the mechanisms of intranasal obstruction in BOAS patients and consequently the treatment modalities. [41]

RFVTR Procedure and Diagnostic Imaging Findings

Mild complications after RFVTR consist of serous nasal discharge during the first week and symptoms of nasal congestion (intermitted stertor and laboured breathing) were observed in 24% of the dogs, 2-3 postoperatively [34]. RFVTR of thin turbinates, turbinates with rhinitis and overtreatment should be avoided to prevent long-term complications like chronic rhinitis and necrosis. Based on the regenerative nature of nasal turbinates, repetitive treatments are to be expected. Finding the patients in need of another turbinoplasty, without regular endoscopy controls is challenging. Obstructive nasal pathways caused by MCPs anecdotical were thought to elicit stertor. In our experience, neither the physiologically occurring periodical obstruction of alternating nasal chambers during the nasal cycle nor the pathological changes by MCPs can be picked up acoustically during routine clinical exams. The most important clinical sign for recurrence of hypertrophic turbinates would be a decrease in cooling ability of the dog, and we suggest that owners should be instructed accordingly. We observe hypertrophy of the dorsal (nasal) turbinate with complete obstruction of the dorsal meatus in our patients on a regular basis. The dorsal meatus serves as a unidirectional fast lane to the olfactory recess. We assume, that reinstallation of a dorsal meatus by turbinoplasty contributes to improving olfaction in dogs with BOAS. Since correction of stenotic nares serves the same purpose, objective evaluation of that effect remains difficult.

Follow-up

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