Two of the most common diseases affecting the upper airway of the dog are brachycephalic airway syndrome and idiopathic laryngeal paralysis. There should be no confusion between the laryngeal collapse seen in brachycephalics, and laryngeal paralysis seen in large breed dogs. Although both conditions may present as upper airway emergencies, they are quite separate disease entities.

Brachycephalic Syndrome

The brachycephalic breeds have been selectively bred for a flat face, but soft tissues have not been condensed proportionately to their foreshortened skulls. This has resulted in:

 Excess nasal and oropharyngeal mucosae;

 A thick, redundant soft palate which interferes with laryngeal function; and

 Shortened, medially displaced nasal cartilages covered with thickened epithelium, resulting in functional stenotic nares.

These are the primary anatomical changes that cause chronic upper airway resistance and obstruction, increased inspiratory effort and marked negative pressures on inspiration.

The high negative inspiratory pressures and air turbulence cause edema, inflammation and stretching of redundant tissues, and eventually laryngeal collapse. There is also strain on lung mechanics from greater changes in intrapleural pressure. The resultant increase in pulmonary resistance (attributed to increased tone in bronchial smooth muscle), can lead to cor pulmonale. In some breeds, especially bulldogs, clinical signs can be further exacerbated by tracheal hypoplasia. Even apparently normal brachycephalics will often show some stertorous breathing, especially when stressed. They have a tendency to open-mouth breathe, are prone to hyperthermia due to poor heat regulation (lack of air flow over the lateral nasal glands), have poor exercise tolerance, and may gag and cough when eating and drinking (due to the thickened and elongated soft palate). They often show signs of sleep disordered breathing and may have chronically low O₂ saturation levels, and thus be polycythemic. Chronic GI disease has been reported in these dogs (gastroesophageal reflux, gastric retention, pyloric hyperplasia and stenosis).

Affected dogs can present to the veterinarian with a range of clinical signs, from mild to severe respiratory distress. The history is usually chronic, with variable signs of mouth breathing, stertor, exercise intolerance, gagging, dysphagia. Animals are prone to decompensation from various precipitating factors such as stress, excitement, exercise, high ambient temperatures, sedation. These cases can develop severe stertor, hyperthermia, tachypnea, tachycardia, cyanosis, and collapse. Emergency treatment should be initiated immediately upon recognition of the situation: allow patient stay sternal; oxygenate; cool down; intravenous fluids; sedation; corticosteroids. Occasionally anesthesia, endotracheal intubation then temporary tracheostomy is required.

Diagnosis is usually obvious from signalment, history, clinical signs and physical examination. Radiographs should be taken to evaluate pharynx, larynx, trachea, lungs and heart (these breeds can also have congenital cardiac defects). Routine labs are indicated in older or more acutely compromised patients. Endoscopic evaluation of the esophagus, stomach, and duodenum with biopsies may be indicated in dogs showing gastrointestinal signs. Confirmation of elongated soft palate and evaluation of the larynx usually occurs at induction of anesthesia for surgery. In affected dogs, the soft palate is seen overlying most of the epiglottis (in normal dogs, it should be just at the tip), and sometimes extending into the rima glottidis. The mucosal saccules lining the laryngeal ventricles will be everted in animals with any prolonged history--this is regarded as the first stage of laryngeal collapse, and is present in over half the cases presented. These edematous, everted saccules sit at the base of the glottis, immediately rostral to the vocal folds. The second stage of laryngeal collapse is aryepiglottic collapse (cuneiform process and aryepiglottic fold deviate toward the midline); followed by corniculate collapse (the corniculate processes rotate and collapse ventro-medially, touching each other, and the cuneiform processes tend to overlap).

Treatment is aimed at surgically relieving upper airway obstruction and eliminating exacerbating conditions. It is preferable to operate in the first year of life to minimize progression of secondary changes. Atraumatic surgical technique will limit post-operative edema, which can be quite dramatic. Correct positioning greatly facilitates surgery--sternal recumbency with maxilla hung, mouth secured open, and lips retracted.

Partial resection of the soft palate (staphylectomy, palatoplasty): The soft palate is ideally resected to be level with the caudal pole of the tonsils. There are several techniques described for resecting the overlong soft palate in brachycephalic dogs.

Excision of everted laryngeal saccules: The saccule is grasped with a long handled, fine-tipped instrument, retracted rostrally and amputated at its base with long handled scissors, carefully avoiding the vocal folds. Temporary extubation may be required.

Rhinoplasty: A cuneiform wedge resection of the dorsal parietal cartilages can be performed and the cut edges apposed with fine suture material. There are several modifications of the wedge resection, an alapexy technique, and some just amputate the dorsal parietal cartilage.

Post-operative monitoring is critical, with oxygenation and late extubation recommended. One should be prepared to re-intubate quickly, with intravenous anesthetic agents drawn up and the I/V catheter still in place. If marked post-operative edema is causing respiratory embarrassment, racemic epinephrine can be nebulized. Only occasionally will a temporary tracheostomy tube be required. Swelling usually resolves within 24 hours. Animals with a history of regurgitation will benefit from antiemetic and antacid medication.

The prognosis depends on the degree of primary changes and the severity of secondary changes at the time of surgery. The young, mildly affected patient may not show marked improvement post-operatively, but the long-term prognosis is better as secondary changes are less likely to develop. In clinically affected patients without advanced laryngeal collapse, widening the nares, shortening the soft palate and excising the everted laryngeal saccules should relieve moderate to severe signs of respiratory distress. These patients will breathe with less effort, will be more tolerant of exercise and excitement, and should make less noise. Animals with more advanced laryngeal collapse do not respond as well to surgical resection of the above redundant tissues, although some respiratory distress may be alleviated. If signs are not adequately ameliorated following nares, soft palate and laryngeal saccule resections, subglottic laryngoplasties with vocal process lateralization can be performed, but most recommendations are to perform a permanent tracheostomy.

Post-operative complications can include: some transient dysphagia, gagging and coughing. More serious complications include: voice changes are due to vocal cord damage, rhinitis from overshortening of the soft palate. The latter complication can be surgically addressed with buccal mucosal flaps.

Idiopathic Laryngeal Paralysis

It is critical to know the anatomy and dynamics of the larynx, because complete exposure may not be attainable during surgery on this structure. The rima glottidis is the narrowest part of the larynx, thus its size will determine the rate at which air can be passed into and out of the lungs. The glottis is widened by abduction of the arytenoids as they rotate around the cricoarytenoid articulation upon contraction of just one muscle, the dorsal cricoarytenoideus. The glottis can also close very tightly when required (swallowing, laryngospasm, coughing, parturition) by the ventromedial rotation of the arytenoids, upon contraction of the cricothyroideus, lateral cricoarytenoideus, and thyroarytenoideus, thus adducting arytenoids and tensing the vocal cords. The larynx maintains a patent airway while supporting two sets of valves, the passive, hinged epiglottis, and the active glottis. All muscles, apart from the cricothyroideus, are innervated via the recurrent laryngeal nerve. The larynx regulates airflow and minimizes resistance to passage of air when demand is increased: at rest: slight abduction of arytenoids during inspiration, passive relaxation during expiration; with vigorous exercise: maximal abduction during inspiration and expiration.

Although inherited, traumatic and iatrogenic laryngeal paralyses are occasionally seen, by far the most form is an idiopathic degeneration of the recurrent laryngeal nerves, termed idiopathic laryngeal paralysis (ILP). Neoplasia and polyneuropathies must also be ruled out before an idiopathologic diagnosis is made. Loss of transmission of impulses through the recurrent laryngeal nerve (to the caudal laryngeal nerve) results in denervation atrophy, and a flaccid paralysis. Increased resistance to airflow through the glottis causes turbulent airflow over the mucosa leading to edema and hyperemia, further compromising the patient. ILP has an insidious onset and progression, so depending on the activity level of the dog; the disease may not manifest itself clinically to the owner until quite advanced. ILP is seen typically in older, usually male, medium to large breeds. The condition is bilateral by time of diagnosis. A change in bark may be the first sign, but all cases will have inspiratory stridor and decreased exercise tolerance. Exertional dyspnea, gagging while eating or drinking, and a soft cough are also common. Stressors such as hot weather, car rides, excitement, can lead to tachypnea, dyspnea, cyanosis, tachycardia, hyperthermia and collapse.

ILP can be highly suspected by signalment, history and clinical presentation. A complete physical and neurological examination should be performed, ruling out other causes of paralysis or airway compromise. Thoracic and neck radiography is essential to rule out masses, tracheal disease, aspiration pneumonia, megaesophagus. Secondary cardiac changes, hiatal hernia and gastroesophageal reflux can be seen associated with ILP. All cases should undergo routine hematology, biochemistries, urinalysis, and thyroid panel. AChR antibody titer may be done if myasthenia gravis is suspected. A positive contrast esophagram will identify any concurrent esophageal dysfunction. Diagnosis is usually confirmed via laryngoscopy under a sub-anaesthetic bolus of thiopental or propofol. The larynx should be observed closely for a long period, matching any movement to the phase of respiration.

Normal: inspiration = symmetric slight abduction of arytenoids; expiration = relaxation of arytenoids to rest in paramedian position

Paralyzed: inspiration and expiration = vocal folds and arytenoids remain in paramedian position. May see paradoxical movement, or flutter, or fasciculations. The mucosa is often hyperemic and edematous. Doxapram HCl is effective at stimulating breathing (1-5mg/kg IV, can be repeated) in apneic animals.

Other diagnostics that have been reported include ultrasonography, transnasal laryngoscopy, electromyography, and histopathology of the DCA muscle taken in surgery. Tidal breathing flow-volume loop and arterial blood gas analyses have been used experimentally to evaluate outcomes.

Treatment of the acutely distressed patient is similar to the decompensated brachycephalic. Fluid therapy should be careful until status of heart, lungs and kidneys are known.

The patient should be observed closely. Very occasionally, complete airway obstruction develops. In these cases, intravenous anesthesia can be administered, laryngeal exam, intubation, radiography, and then either temporary tracheostomy or definitive surgery can be performed. It is ideal to delay definitive surgical correction until the animal has stabilized and all diagnostics have been completed.

Many different surgical treatments for laryngeal paralysis have been described over the years. The most common procedure is some form of unilateral arytenoid mobilization. This technique alleviates signs consistently, effectively and immediately, is simple to perform, has a relatively low complication rate, and is not radical or invasive. Two basic variations of arytenoid mobilization have been reported--either a cricoarytenoid laryngoplasty (= abduction of the arytenoid), or thyroarytenoid lateralization (= lateral and caudal displacement of the arytenoid), or a combination of both. There is little difference in clinical outcome between techniques. Further modifications include variation on the degree of cricothyroid disarticulation, transection of the interarytenoid cartilage, and suture tension. Complete disarticulation of the cricothyroid joint weakens the lateral support to the larynx, and it should be discouraged. Adequate exposure can be obtained without CT disarticulation. Transection of the interarytenoid cartilage distorts the rima glottidis, and is not necessary with cricoarytenoid laryngoplasty. Suture tension should not be excessive, as the arytenoids are already somewhat abducted from the endotracheal tube, and high suture tension may increase the incidence of post-operative aspiration pneumonia. If the cartilages are calcified, they could fragment, so extra should be taken when penetrating the muscular process.

The overall advantages of the arytenoid mobilization are a consistent increase in lumen size, with good clinical results. The technique does not require tracheostomy, there is a low risk of intraglottic scar formation, and it is a quick procedure to perform.

Most dogs have an improved quality of life following surgery, with significantly reduced upper airway obstruction. Minor complications include seroma formation, some coughing associated with eating/drinking, and occasionally only moderate improvement in exercise tolerance. The major post-operative complication is post-operative aspiration pneumonia, with some reports up to 24%. Factors associated with increased risk of developing complications include: preoperative aspiration pneumonia, postoperative megaesophagus, temporary tracheostomy placement, and concurrent neoplastic disease, and possibly size. Cases that present with aspiration pneumonia post-operatively (sometimes months after surgery) can generally be treated successfully, although some patients will have recurrent episodes. We are currently concluding a prospective, long-term cohort study looking at risk factors for development of aspiration pneumonia, which runs at 6% in our hospital.

Surgical intervention for idiopathic laryngeal paralysis results in a high level of owner satisfaction, providing a significantly improved quality of life for most of these elderly patients.