Brachycephalic airway obstructive syndrome (generally shortened to brachycephalic syndrome) encompasses a group of anatomic abnormalities that can result in severe inspiratory stridor. Most commonly identified abnormalities include stenotic nares (Figure 1), elongated soft palate and everted laryngeal saccules. Respiratory distress can be further complicated by enlarged tonsils, narrowed rima glottidis, tracheal hypoplasia and/or tracheal collapse and laryngeal collapse. Brachycephalic breeds such as the English and French bulldog, Boston terrier, pug, boxer, Shih Tzu and Pekingese are over-represented, but any dog with a skull width: skull length ration of 0.81 or greater is predisposed to BAOS.
Stenotic nares are usually present at birth, but often patients are not presented for clinical signs related to BAOS until 2-4 years of age. Dogs with BAOS may present as stable patients with a history of “snoring” or noisy breathing, interrupted sleeping, and vomiting not related to meal time and mild exercise intolerance. Other dogs may present in fulminant respiratory distress often complicated by heat stress. A history of a typical BAOS patient includes stertor and/or stridorous breathing which worsen with exercise and excitement, restless sleeping, gagging and/or retching sometimes associated with swallowing, and collapse. Obesity, heat and humidity, exercise and excitement worsen clinical signs.
The pathophysiology of this syndrome is both simple and complex. From a simplistic view, all of the anatomic changes contribute to airway narrowing and thus increased inspiratory resistance. Treatment aims at opening the airway and decreasing resistance.
The complex nature of brachycephalic syndrome is apparent when considering the chronic effect of increased inspiratory resistance on the rest of the dog. Increased inspiratory resistance, i.e. increased negative pressure during inspiration, results in soft tissues being drawn into the airway lumen. Everted laryngeal saccules are commonly seen. These delicate structures can become hyperplastic further narrowing the airway and worsening turbulent airflow. The soft palate, which may be elongated at birth, is stretched caudally and sucked into the airway with each inspiration. The palatine tonsils can similarly become enlarged and pulled into the oropharynx during inspiration. Any of these soft tissue structures can result in ulceration within the larynx, further worsening the cycle of inflammation.
The most advanced stage of BAOS culminates in laryngeal collapse. Loss of rigidity of cartilages (cuneiform and corniculate primarily) and stretching of the soft tissues allow midline collapse of the larynx and for the cartilages to be drawn medially. Laryngeal collapse is a progressive process with worsening prognosis over time.
Severe upper airway resistance can result in pulmonary edema, inadequate pulmonary ventilation and reduced arterial oxygen content. Chronic hypoxia incites pulmonary vasoconstriction and ultimately right-sided heart failure. The effort required by affected dogs to move air in the face of airway obstruction can result in an abdominal component to inspiration which predisposes the patient to regurgitation, aspiration pneumonia and hiatal hernia.
Diagnosis includes cervical and thoracic radiographs, complete blood count and serum biochemical analysis, venous blood gas analysis, and oropharyngeal and laryngoscopic exam. In a stable patient, diagnostics can be performed in a stepwise fashion depending upon owner wishes. However in the case of acute respiratory distress, a single anesthetic episode (for radiographs, airway exam and possible surgical intervention) is preferred due to the risk of anesthetic complications. The upper airway laryngoscopic exam is performed under light general anesthesia with the goal of minimizing the anesthetic effect upon airway function. This hospital generally uses an opiod premedication (hydromorphone or oxymorphone) followed by propofol IV for induction. Key areas to evaluate during examination include palatine tonsils, soft palate length, laryngeal saccules, rima glottidis, function of laryngeal cartilages, and overall impression of inflammation.
Thoracic and cervical radiographs are indicated to look for tracheal collapse or hypoplasia, megaesophagus, aspiration pneumonia, pulmonary edema, hiatal hernia and any other lesions that may contribute to respiratory distress. Tracheoscopy and bronchoscopy are indicated if tracheal collapse is the part of the clinical presentation.
Some dogs that present in acute respiratory distress may require immediate anesthetic induction and intubation in order to provide adequate oxygen and help control hyperthermia. An anti-inflammatory dose of a fast acting corticosteroid to address acute swelling in the larynx is indicated and dogs are maintained intubated under a propofol continuous rate infusion. For less severely affected patients, sedation (opiod and benzodiazepine) and placement in 100% oxygen may be enough to break the respiratory distress cycle. Hyperthermic dogs should be cooled with topical isopropyl alcohol and fans.
Surgical treatment for BAOS includes wedge resection of the wing of the nostril, staphylectomy and laryngeal saccule resection. There is evidence that surgically widening the nostrils of young brachycephalic breeds prior to developing clinical signs of BAOS may improve their long-term prognosis. Some surgeons recommend nostril wing wedge resection (sometimes referred to as alar fold resection) of all brachycephalic breeds demonstrating stenotic nares within the first year of age. Potential implications for show and breeding animals should be discussed with owners before undertaking any prophylactic surgery such as alar fold resection. Staphylectomy, resection of the caudal edge of the soft palate, in these young, non-clinical patients is less clearly advantageous. Everted laryngeal saccules are excised via an oral approach. Resection of the tonsils in clinically affected patients may be indicated if the tonsils protrude from their crypts, however they rarely contribute to airway resistance due to their oropharyngeal location. Each of these procedures can be performed with surgical laser, rather than traditional instrumentation. Electrosurgery should be avoided due to increased soft tissue inflammation and decreased cosmesis. Post-operatively, dogs are recovered in oxygen with delayed extubation or a temporary tracheostomy if necessary. Antibiotics and sedation are given according to the individual case. Most dogs remain in hospital 24-48 hours after surgery to monitor for respiratory distress.
For animals with stage 2 or 3 laryngeal collapse, permanent tracheostomy is recommended. Arytenoid lateralization and partial arytenoidectomy have not shown favorable results in these severely affected individuals. In dogs with tracheal collapse, tracheal stenting may be required to significantly reduce the airway resistance. In dogs with tracheal hypoplasia, such as English and French Bulldogs, it is important to determine if collapse is present as stenting will not improve a congenitally narrow trachea.
Prognosis for young dogs undergoing surgery is good providing owners can reduce risk of hyperthermia and respiratory distress. Weight reduction should be implemented for obese dogs. Avoiding heat stress, humidity and environments with high particulate contamination is important with both surgical and medical management. Prognosis for dogs managed medically is guarded with recurrence of acute respiratory distress common. BAOS, which has progressed to laryngeal collapse, carries a guarded prognosis even with surgery to create a permanent tracheostomy.
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