Dale E. Bjorling, DVM, MS, DACVS
Dogs and cats with brachycephalic conformation of the skull are prone to multiple abnormalities of the upper airways. Although these disorders are mostly seen in small brachycephalic dogs (English Bulldogs, Pugs, etc), these abnormalities can occur in larger dogs (St. Bernards, Mastiffs, etc.) or cats which tend towards brachycephalic conformation (Persian and Himalayan). Brachycephalic airway syndrome refers to upper respiratory obstructive resulting in increased resistance to air flow. Assessment and surgical treatment should encompass all structural abnormalities that may be contributing to increased airway resistance.
One or more of the following disorders are usually seen in these animals: stenotic nares, elongated soft palate, everted laryngeal saccules and tracheal hypoplasia. In some animals, further abnormalities of the airway due to cartilage defects may be seen such as collapsing trachea and laryngeal collapse. In a very few instances, grossly enlarged tonsils may contribute to the airway obstruction. It has been suggested that the conformation of the brachycephalic skull predisposes these animals to abnormalities of the upper airways due to impingement of tissue on the pharynx.
Brachycephalic animals with upper airway abnormalities will be examined for evaluation of varying degrees of respiratory distress. Respiratory distress may often be exacerbated by excitement, hyperthermia, or other stress but is usually present at some level at all times. Initial treatment in severely affected animals should focus on increasing systemic oxygenation and reducing oxygen consumption by administration of supplemental oxygen and sedation.
Diagnosis of specific airway abnormalities in an individual patient requires thorough evaluation of the nares, oral and nasal pharynx, and larynx. This examination will require induction of a light plane of anesthesia with intravenous propofol or pentothal. It is not uncommon that animals with airway abnormalities associated with brachycephalic skull conformation have difficulty recovering from anesthesia, and it may be necessary to surgically correct airway abnormalities as an emergency procedure to facilitate recovery from anesthesia. Upper airway obstruction of long-standing duration is also thought to lead to laryngeal collapse in some animals due to weakening of the laryngeal cartilages as a result of chronic exposure of the larynx to high negative pressures as the animal struggles to breathe against increased airway resistance.
Congenital stenosis of the nares usually occurs bilaterally, but traumatic injuries can result in unilateral stenosis. Stenotic nares prevent effective nasal breathing and increase overall airway resistance. The goal of surgery for animals with brachycephalic airway syndrome is an overall reduction in airway resistance so correction of stenotic nares is usually part of a package of surgeries directed to this purpose. Surgical correction entails removal of a wedge of the alar wing lateral to the naris to increase airflow. The exact positioning of the wedge relative to the curvature of the lateral aspect of the naris is variable and should be placed to achieve maximal lateral and dorsal rotation of the alar wing and enlargement of the naris. It should be noted that the primary area for air passage through the naris is dorsal. Thus, a procedure that only lateralizes the ventral alar wing is of reduced effectiveness. In rare instances, a more aggressive approach that debulks the intranasal portion of the alar fold may be used to further open the airway in this area.
Primary goals of the surgery include achieving a satisfactory opening of the nares, maintaining a symmetric appearance, and precise suture placement to facilitate healing and minimize the development of a nonpigmented scar. Using a scalpel blade, a triangular wedge of tissue is removed from the lateral aspect of the naris. The midpoint of the base of the triangle should approximate the point of maximal curvature of the lateral cartilage. Resection of tissue should be carried sufficiently caudal to increase the airway diameter. Hemorrhage is brisk but can be controlled with pressure and closure of the wound. Closure is achieved with a fine gauge (4-0) monofilament nonabsorbable suture placed in a simple interrupted pattern, taking care to accurately appose the pigmented tissues. Opening of the dorsal naris can be improved by using an asymmetric suture placement technique. This is accomplished with the first suture and if the results are satisfactory the remaining sutures are placed in a direct appositional manner. Asymmetric suture placement is done by taking a bite of the lateral wound edge more cranially than is the bite on the medial wound edge. Tightening of this suture results in lifting the alar wing in both a lateral and a dorsal direction, achieving better opening in the dorsal naris region. Sedation is usually required to remove sutures.
Surgical manipulation of the pharynx or excision of the soft palate may stimulate the animal to vomit after recovery from anesthesia. Furthermore, the brachycephalic conformation and postoperative swelling may predispose to aspiration if vomiting does occur. Thus, premedication with metoclopramide (0.2–0.4 mg/kg IM or SC) may be prudent.
The caudal border of the soft palate is normally at, our immediately rostral to, the tip of the epiglottis. If the soft palate is longer than this, it frequently will be drawn into the rima glottidis and obstruct airflow through the larynx. During resection of the soft palate, it is difficult to determine the position of the palate relative to the epiglottis. Therefore, it is better to use the caudal border of the tonsillar crypts as the landmark for resection. Although electrocautery or CO2 laser has been recommended to diminish hemorrhage during palate resection, hemorrhage is seldom a serious complication of resection of elongated soft palate. The use of electrocautery to excise the soft palate is not recommended due to the subsequent occurrence of increased swelling. With the endotracheal tube in place, the caudal border of the soft palate is grasped with thumb forceps and pulled rostrally. At this point, the palate can either be clamped with hemostats to set the line of excision or can be cut free hand with no clamping. If a clamp method is used, curved or right angle forceps are applied across the soft palate at the level of the caudal border of the tonsillar crypts. These are left in place for 3–5 minutes. If the surgeon is right-handed, the forceps on the animal's left side is removed first, and an incision is made with curved scissors through the crushed mark created in the soft palate. The resulting defect is closed with absorbable suture material (the author's preference is 4-0 or 5-0 braided absorbable material such as Vicryl) in a simple continuous pattern placed in the dorsal and ventral mucosa of the soft palate. After the initial incision is partially closed, the remaining forceps is removed, and the incision is completed across the soft palate. The defect is closed by continuing the initial suture line. It is not uncommon that increased hemorrhage will occur laterally near the tonsillary crypts. While this is usually controlled by suture placement used to close the defect in the soft palate, ligatures must occasionally be applied to control hemorrhage. In some cases, the excess palate tissue tracks down the pharyngeal wall as an excess fold of tissue. In these cases the line of excision is continued along the fold and it is closed as part of the palate suture line closure.
Alternatively, the soft palate can be resected free hand without placement of crushing forceps prior to excision. Only slightly more hemorrhage is encountered when this step is omitted. If a free hand cut is made, it is useful to cut one side and complete the suturing on that side before doing the second half. This approach can help to prevent the line of excision from straying as it is made. To start the incision, the caudal tip of the soft palate is grasped with forceps and drawn rostrally. A cut is made in the center of the palate at the level of the caudal tonsillar crypt to mark the level of excision and an incision is made half way across the palate. The resulting defect is closed as described previously, the incision is then extended to include the entire width of the soft palate, and the suture line is completed. If excess pharyngeal folds need to be included the excision lines can be extended along with the initial cut to include them.
It is unlikely that everted laryngeal saccules occur as a congenital abnormality. Eversion of the laryngeal saccules is the result of prolapse of the mucosa lining the laryngeal crypts rostral to the vocal folds due to excess negative pressures during respiration and may be the first manifestation of laryngeal collapse. In all probability, eversion of the laryngeal saccules is the result of turbulent airflow created by narrowing of the upper airway and the increased negative pressure generated within the larynx during inspiration in an attempt to overcome upper airway resistance. The laryngeal saccules are normally not visible when the larynx is viewed through the mouth; however, in brachycephalic dogs, they often become edematous and appear as gray, somewhat gelatinous masses rostral and ventral to the vocal folds and. Although detection and evaluation of everted laryngeal saccules by ultrasonography has been described (Rudorf 1999), eversion of the laryngeal saccules is most often diagnosed during evaluation of the oral cavity, pharynx, and larynx while the animal is lightly anesthetized. The laryngeal saccules may touch on the midline. These can be excised with a curved scissors. Hemorrhage is usually not observed. If hemorrhage occurs, this can be controlled by application of direct pressure using a cotton tipped applicator for 4 to 5 minutes.
Laryngeal collapse may also be seen in brachycephalic dogs and is often significantly exacerbated if large everted laryngeal saccules are present. Laryngeal collapse has a variable degree of severity but is often seen in its milder form as a combined dorso-ventral and latero-medial collapse of the rima glottidus. The corniculate processes are often in contact so the dorsal rima glottidus is obstructed and air flow is only possible ventrally. Severe collapse will present with overlap of the cartilages and poor structural rigidity of the laryngeal cartilages. There is no current direct treatment for laryngeal collapse and in the best case scenario (assuming a normal trachea) is to bypass the larynx with a permanent tracheostomy.
Tracheal hypoplasia is infrequently observed in cats or larger brachycephalic dogs. In one retrospective study of 103 dogs with congenital tracheal hypoplasia, Bulldogs (55%) and Boston Terriers (15%) were the most commonly represented breeds, and this disorder appeared to be more common in males (66%) than females (34%). Interestingly, tracheal hypoplasia was accompanied by elongated soft palate in only 43%, and stenotic nares in only 22%, of the dogs studied, suggesting that these defects may occur independently. Dyspnea is classically associated with tracheal hypoplasia; however, not all affected dogs will be dyspneic, and tracheal hypoplasia may be diagnosed incidentally on thoracic radiographs made for other reasons. Unfortunately, there is no effective means of treatment. Medical management is minimally effective if this abnormality is severe.