Tracheal Collapse

The primary function of the trachea is to serve as a conduit for air into and away from the bronchial tree. Tracheal collapse occurs when there is malacia of the tracheal cartilages leading to varying degrees of dorsoventral flattening, impeding airflow. Controversy exists over management of tracheal collapse as medical management is directed only at symptomatic therapy, and surgical treatment is burdened by complications.

Functional Anatomy

The trachea of the dog or cat is composed of 35 to 45 incomplete C-shaped cartilage rings, although variations may exist between breeds and individual animals [1,2]. The ends of the cartilages are connected by the dorsal tracheal membrane, which is the thin, strap-like muscle on the dorsal surface of the trachea. The first tracheal ring is complete and partially covered by the cricoid cartilage. The remaining tracheal rings are linked together by elastic annular ligaments that result in the rigid, yet flexible tube.

The blood supply to the trachea is from the cranial thyroid artery, caudal thyroid artery, and bronchoesophageal arteries. Branches of the thyroid arteries penetrate the tracheal rings on either side and then arborize in the submucosa to create a rich subepithelial plexus in the cervical and proximal thoracic trachea. Branches of the bronchoesophageal arteries supply the terminal trachea, carina, and mainstem bronchi. The trachea is innervated by the autonomic nervous system; stimulation results in muscle contraction and glandular secretion.

The trachea is composed of four distinct layers: mucosa, submucosa, musculocartilaginous layer, and adventitia [3]. The mucosa is made up of pseudostratified, ciliated, columnar epithelium and goblet cells, and is oriented in longitudinal folds. Tracheal glands within the submucosa contribute mucus to respiratory secretions. The musculocartilaginous layer is composed of hyaline cartilage, fibroelastic tissue, and smooth muscle that blend with the connective tissue of the adventitia.

The main function of the trachea is to channel air through the phases of respiration. The lumen diameter of the trachea is capable of changing in size by contraction of the dorsal tracheal membrane. Muscle contraction brings the ends of the incomplete cartilage rings closer together, narrowing the diameter, and thus reducing ventilatory dead space and increasing airflow velocity. The tracheal diameter can also enlarge to accommodate increases in airflow volume and reduce airway resistance. Insult to the tracheal wall can affect how the trachea adapts to changes in airflow and external pressures. Airflow velocity increases as diameter decreases and, according to the Bernoulli effect, internal pressure decreases. A normal trachea is rigid enough to withstand external pressure, but weakened tracheal cartilages are subject to collapse.

Another important role of the trachea is to trap aspirated debris and transport this material back up the tracheobronchial tree. The mucociliary apparatus is responsible for clearance of small particles (1 to 5 µm) that are able to pass through the nasopharynx [4]. These particles adhere to the mucus lining of the large airways; cilia of the epithelial cells beat in the mucus layer, pushing material back toward the pharynx. Normal cilia beat at a rate of 15 to 20 times per second, resulting in a clearance time in the normal dog of 5 to 26 mm per minute [5]. The mucociliary apparatus and clearance rate can be markedly affected by airway disease and mucosal trauma.

Pathophysiology

Tracheal collapse results from structural abnormalities of the cartilage rings and secondary changes in the dorsal tracheal membrane. Histopathology and ultrastructural analysis of tracheal cartilage in dogs with tracheal collapse found hypocellularity leading to decreased chondroitin sulfate and glycosaminoglycans and transformation of normal hyaline cartilage to fibrous cartilage [6]. This chondromalacia makes the trachea less rigid and less able to withstand external pressures, resulting in dorsoventral flattening. The specific etiology of tracheal collapse is unknown but is thought to be multifactorial with a congenital or inheritable component [7].

Tracheal collapse may be confined to an isolated segment or may involve the entire trachea and bronchial tree. The thoracic inlet is the most commonly involved area (Fig. 53-1). Collapse typically occurs in a dorsoventral direction as the cartilages weaken and the dorsal tracheal membrane thins and lengthens; however, lateral collapse of the tracheal walls has been reported [8].

Figure 53.1. Lateral thoracic radiograph showing severe tracheal collapse at the thoracic inlet.

Collapse in the cervical tracheal and thoracic inlet classically occurs on inspiration as pressure within the lumen drops and the walls are susceptible to atmospheric pressure; intrathoracic trachea collapses on expiration. Although pressure within the trachea decreases on inspiration, luminal pressure still exceeds intrapleural pressure, which keeps airways open. On expiration, intrapleural pressure becomes less negative and exceeds intraluminal pressure. Dogs with weakened cartilages lack sufficient strength to withstand the increased intrapleural pressure. The thoracic inlet is most susceptible to tracheal collapse as this is the site of the equal-pressure point: where intrapleural pressure equals intraluminal airway pressure and where the transition from intrapleural to atmospheric pressure occurs [7]. One study, however, found occasional evidence of dogs that had intrathoracic collapse on inspiration and extrathoracic collapse on expiration, although no explanation could be offered [9].

Dogs with tracheal collapse have varying degrees of secondary injury owing to chronic coughing. Coughing causes further increase in intrapleural pressure and worse tracheal collapse. In cases of moderate to severe collapse, opposing epithelial linings come into contact causing mucosal lesions and irritation. This chronic irritation leads to inflammation, mucus gland hyperplasia, epithelial desquamation, and disruption of the mucociliary clearance [7].

Signalment/Presentation

Tracheal collapse is typically associated with middle-aged toy and miniature breed dogs. Classic breeds include Yorkshire terriers, toy poodles, miniature poodles, Pomeranians, Chihuahuas, and pugs. This condition has also occasionally been described in young large breed dogs [10,11] and in cats [12-14]. In cats, tracheal collapse has been associated with intraluminal, extraluminal, or nasal masses.

Most dogs are diagnosed around 6 to 7 years of age; however, it has been reported that 25% of affected dogs are symptomatic by 6 months of age [15]. Dogs present with an easily solicited cough that is most often described as a "goose-honk". Severely affected dogs may have exercise intolerance, respiratory distress, and syncope. Clinical signs are exacerbated by stress or excitement.

Dogs with tracheal collapse may suffer from a variety of concurrent problems. Almost 50% of dogs suffer from a degree of obesity that worsens clinical signs [7]. Laryngeal paresis or paralysis has been reported in 20 to 30% of dogs, while one third of dogs have concurrent systolic heart murmurs consistent with mitral valve insufficiency [7,15,16]. Upper respiratory signs may be aggravated by an enlarged left atrium, putting pressure on the carina and mainstem bronchi.

At least 40% of dogs are believed to have a degree of dental or periodontal disease [7]. Aspiration of oral bacteria into diseased airways is hypothesized to contribute to exacerbation of clinical signs owing to increased airway inflammation or increased coughing. In a study of 37 dogs with tracheal collapse, 83% had a positive large-airway culture, with 59% growing greater than one species of bacteria [17]. This is of interest as oropharyngeal flora have been found in the trachea of normal dogs, but only 17% had multiple, mixed colonization [18]. Concurrent cytologic inflammation however, was not consistently found in a population of dogs with tracheal collapse; therefore, an association between bacterial colonization of large airways and clinical signs has not yet been proven [17].

Concurrent hepatomegaly and hepatopathy are also common in dogs with tracheal collapse. In a study of 26 dogs, 46% had increased serum activity of two or more liver enzymes, with 92% having elevated serum basal bile acid concentrations [19]. The reason for this association is still unclear, although speculative theories include passive hepatic congestion or centrilobular liver cell necrosis secondary to chronic hypoxia.

Diagnosis

The diagnosis of tracheal collapse is often suspected based on signalment, history, and physical examination findings. Lateral survey thoracic radiographs of the neck and thorax can confirm this diagnosis. Views should be taken of the cervical and thoracic trachea on both inspiration and expiration. Cervical trachea narrows during inspiration owing to negative pressure within the trachea, whereas intrathoracic trachea collapse occurs during expiration owing to increased intrapleural pressure. Static radiographs may only detect collapse in 59 to 92% of cases [9,15,16] yet radiographs should be closely evaluated for signs of concurrent airway pathology or cardiac disease [7,20]. Dynamic evaluation of the trachea can be performed using fluoroscopy and is particularly helpful for identification of intrathoracic collapse. When comparing fluoroscopy and standard radiographic evaluation, radiography has been found to underestimate the frequency and degree of tracheal collapse.9 Detection of tracheal collapse using ultrasonography has also been described [21].

Bronchoscopy allows direct visualization and evaluation of the entire tracheobronchial tree (Fig. 53-2A). In particular, bronchoscopy allows evaluation of the main stem bronchi (Fig. 53-2B). Airway samples for cytology and bacterial culture can be obtained by tracheal brushing or bronchoalveolar lavage, as tracheobronchitis or bronchopneumonia may play a role in the severity of clinical signs. The disadvantage of bronchoscopy is that general anesthesia is required. However, this provides an opportunity to assess laryngeal anatomy and function.

Figure 53.2. Bronchoscopic view of cervical trachea collapse and left mainstem bronchi (arrow) of the same dog.

Tracheal collapse can been graded by its appearance on fluoroscopy or bronchoscopy (Table 53-1; Fig. 53-3). This grading scheme allows for the determination of the severity of the collapse, establishes a baseline from which to assess disease progression, and identifies or eliminates the potential for surgical intervention.

Figure 53.3. Graphic representation of tracheal collapse grading scheme.

Treatment

Medical management of tracheal collapse results in improvement in most dogs [15]. Weight loss is critical to the success of other medical therapies. Environmental modifications, such as the use of a harness instead of a collar and creation of a nonsmoking environment, may help some dogs, as will management of concurrent underlying conditions. It has also been advocated to perform dental prophylaxis in affected dogs to decrease the bacterial load that can be aspirated into the trachea [7]. Frequently used medications include cough suppressants, bronchodilators, anti-inflammatories, and antibiotics.

Surgical intervention is suggested in patients with moderate to severe tracheal collapse that are refractory to medical management. Surgery is not recommended in patients with mainstem bronchi collapse, underlying laryngeal disease, and concurrent cardiopulmonary disease. Although other techniques have been described, surgical treatment of tracheal collapse is currently achieved by either extraluminal ring prostheses or endoluminal stenting.

Extraluminal tracheal ring prostheses can be implanted in dogs with cervical tracheal collapse or proximal intrathoracic tracheal collapse. Good to excellent outcomes have been reported in 75 to 85% of patients, however, this technique is limited by candidate selection and surgical complications [16,22]. Following surgery, laryngeal paralysis, laryngeal necrosis, and postoperative distress requiring permanent tracheostomy have been reported [22]. Dogs older than 6 years appear to have worse outcomes than younger dogs regardless of the degree of collapse [22].

Endoluminal stenting has been reported in a variety of settings and using a large array of materials [23-25]. Endoluminal stenting can be used in dogs with intrathoracic tracheal collapse or diffuse tracheal collapse to provide rapid relief of clinical signs, and has been used in dogs with coexisting bronchial collapse. Complications reported with endoluminal stent implantation include stent migration, stent fracture, granuloma formation, pneumonia, and chronic coughing [26,27].

Conclusion

Tracheal collapse is a challenging condition to diagnose and treat. Diagnosis is complicated by concurrent illnesses that exacerbate clinical signs, and treatment standards of care have not been established. Appropriate medical management may alleviate clinical signs in a large percentage of dogs affected, however dogs refractory to pharmacologic intervention may benefit from extraluminal or endoluminal support.