How I Treat: Tracheal Collapse When Medical Management Fails
World Small Animal Veterinary Association World Congress Proceedings, 2013
Theresa W. Fossum, DVM, MS, PhD, DACVS
Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX, USA

Upper airway procedures are performed to remove, repair, or bypass areas of obstruction, injury, or disease. Affected animals may have mild to severe respiratory distress. Mild or moderately dyspneic patients initially should be examined from a distance to avoid exacerbating the condition. Open-mouth breathing, abducted forelimbs, labored breathing, and restlessness indicate moderate to severe respiratory distress that may require emergency therapy.

Minimal restraint should be used with severely dyspneic patients, and they should be allowed to maintain the position in which they feel most comfortable. Supplemental oxygen may be given by means of nasal insufflation, tracheostomy tube or catheter, endotracheal intubation, mask (including an Elizabethan collar that has had plastic wrap put over it to form a "cage" over the head), or oxygen cage. Corticosteroids, sedation, or cooling (or all of these) may relieve distress. Sedation may be beneficial for anxious patients (especially those with upper airway obstruction) with moderate to severe respiratory distress. Combinations of intravenous drugs are commonly given; hydromorphone or butorphanol and either acepromazine or diazepam are frequently used in dogs (Table 1).

Table 1. Sedation of severely dyspneic dogs

 Hydromorphone: 0.1–0.2 mg/kg IV, IM, or SC

 Butorphanol (Torbutol, Torbugesic): 0.2–0.4 mg/kg IV, IM, or SC

 Acepromazine: 0.02–0.05 mg/kg, max 1 mg IV, IM, or SC

 Diazepam (Valium): 0.2 mg/kg IV

 Fentanyl plus droperidol (Innovar-Vet): 1 ml/20–40 kg IV or 1 ml/10–15 kg IM

IV: intravenous; IM: intramuscular; SC: subcutaneous.

Diagnosis of upper respiratory disease is based on the history and clinical signs, physical examination findings, hematologic and serum biochemical parameters, radiographs, endoscopy, cytologic studies, culture, or biopsy, or all of these. The history and clinical signs may include abnormal respiratory noises (e.g., cough, inspiratory stridor, wheeze), exercise intolerance, hyperthermia, tachypnea, dyspnea, cyanosis, restlessness, and/or collapse. Gagging and regurgitation of secretions are common with nasopharyngeal, laryngeal, and some tracheal abnormalities. Mucopurulent or bloody discharges are common with obstructive or infectious nasal disease. Voice change may occur with laryngeal paralysis, and dysphagia may be noted with supraglottic obstructions. Subcutaneous emphysema occurs with penetrating laryngotracheal or nasal injuries. Clinical signs may intensify or may be precipitated by excitement, stress, eating, drinking, or high ambient temperatures. Laboratory data should be evaluated to detect underlying metabolic disease and determine the advisability of general anesthesia. Tidal breathing flow volume loops are helpful in classifying obstructions as fixed or non-fixed. Pulmonary function tests, electromyography, and nerve conduction studies are ancillary tests that may indicate pulmonary or neuromuscular disease.

Animals with nasal neoplasia, fungal infection, or foreign bodies may be anemic due to profuse epistaxis. Affected animals should be carefully evaluated for clotting abnormalities by assessing platelet numbers, bleeding from venipuncture sites, or the presence of ecchymosis, petechiation, melena, hematuria, or retinal hemorrhage. If available, coagulative ability may be assessed by determining the activated clotting time, prothrombin time, partial thromboplastin time, and/or mucosal bleeding time. Blood transfusions or purified hemoglobin should be given before surgery if the packed cell volume (PCV) is 20% or lower. Bleeding during rhinotomy may be severe, requiring intraoperative blood transfusion or carotid artery ligation, or both.

A preoperative anti-inflammatory dose of a corticosteroid (dexamethasone [Azium], 0.5–2 mg/kg IV, IM, or SC; repeated administration of dexamethasone can cause gastrointestinal hemorrhage) may reduce nasopharyngeal and upper airway edema secondary to surgical or diagnostic manipulations. Corticosteroids are routinely given for nasopharyngeal and intraluminal laryngeal procedures.


Because the respiratory tract has a normal bacterial flora, prophylactic antibiotics (e.g., cefazolin) frequently are given before surgery. However, animals with normal immune function undergoing short procedures (e.g., nares resection, laryngeal saccule resection, vocal cordectomy) do not need them. Streptococci, Escherichia coli, Pseudomonas spp., Klebsiella spp., and Bordetella bronchiseptica are most commonly isolated from normal dogs. A majority of tracheal cultures are sterile, whereas most pharyngeal cultures are not.

The gram-negative organisms which cause most canine respiratory tract infections are resistant to commonly used antibiotics. Antimicrobial drug selection is best based on cytologic and culture results of tracheobronchial, pulmonary parenchymal, and/or pleural secretions. Bland aerosol therapy (e.g., sterile 0.9% saline) helps loosen secretions and facilitates their clearance in dogs with tracheostomies; addition of antibiotics to the aerosol generally is unnecessary. However, intratracheal or aerosolized antibiotics may be effective in some dogs with chronic respiratory infections. Lipid-soluble antibiotics that contain a benzene ring reach the highest levels in the normal trachea and bronchus; however, increased permeability associated with inflammation allows numerous antibiotics to achieve high levels during infection. Antibiotics commonly recommended for treatment of upper respiratory disease include ampicillin, fluoroquinolones, cephalosporins, aminoglycosides, doxycycline, azithromycin, and potentiated sulfonamides.

Tracheal Collapse

The etiology of tracheal collapse is unknown and probably multifactorial. Proposed etiologies include genetic factors, nutritional factors, allergens, neurologic deficiency, small airway disease, and cartilage matrices degeneration. Affected tracheal cartilages become hypocellular, and their matrices degenerate. Normal hyaline cartilage is replaced by fibrocartilage and collagen fibers, and the amounts of glycoprotein and glycosaminoglycans are diminished. The cartilages lose their rigidity and ability to maintain normal tracheal conformation during the respiratory cycle. They usually collapse in a dorsoventral direction.

The cervical trachea collapses during inspiration, and the thoracic trachea collapses during expiration. Collapse reduces the lumen size and interferes with airflow to the lungs. Abnormal respiratory noises, exercise intolerance, gagging, and varying degrees of dyspnea occur with tracheal collapse. Chronic inflammation of the tracheal mucosa causes coughing, which exacerbates inflammation. Persistent inflammation leads to squamous metaplasia of the respiratory epithelium and interferes with mucociliary clearance; therefore, coughing becomes an important tracheobronchial clearing mechanism.

Although the clinical signs may be similar, tracheal collapse should not be confused with tracheal stenosis. Tracheal stenosis is an abnormal narrowing of the tracheal lumen caused by congenital malformation or trauma. Trauma (e.g., penetrating or blunt wounds, foreign bodies, indwelling tubes) or surgery may cause segmental tracheal stenosis when the wound heals by second intention and excess fibrosis and scarring cause luminal narrowing, or tracheal cartilages heal with an abnormal shape. Traumatic stenosis is treated by balloon dilation or resection and anastomosis. Congenital stenosis occurs when tracheal cartilages are abnormally small, abnormally shaped, or malpositioned. Tracheal hypoplasia is a form of congenital tracheal stenosis. It is characterized by an abnormally narrow lumen along the entire length of the trachea, rigid tracheal cartilages that are apposed or overlap, and a dorsal tracheal membrane that is narrow or obscured. Tracheal hypoplasia primarily affects brachycephalic breeds, especially English bulldogs, which sometimes have other congenital abnormalities (e.g., stenotic nares, elongated soft palate, aortic stenosis, pulmonic stenosis, megaesophagus). Tracheal hypoplasia can be associated with continuous respiratory distress, coughing, and recurrent tracheitis but may be tolerated in the absence of concurrent respiratory or cardiovascular disease. Tracheal hypoplasia can be identified endoscopically or radiographically. Treatment of tracheal hypoplasia is symptomatic medical therapy (i.e., antibiotics, cough suppressants) and correction of other airway obstructions (e.g., resection of nares, palate, saccules).

Surgical Treatment

Surgery is recommended for all dogs with moderate to severe clinical signs, a 50% or greater reduction of the tracheal lumen, or clinical signs refractory to medical therapy (Figure 1). Surgery should not be delayed until the animal is in severe respiratory distress. Tracheal collapse often is overlooked in young dogs, which allows degenerative changes to progress, clinical signs to worsen, and secondary problems to develop. Dogs presented for treatment with laryngeal paralysis or collapse, generalized cardiomegaly, bronchial collapse, and chronic pulmonary disease are poor surgical candidates. Coughing and dyspnea caused by laryngeal, pulmonary, or cardiac disease are not expected to improve without appropriate therapy. Respiratory distress and death may occur in animals with severe laryngeal dysfunction or bronchopulmonary disease. Concurrent mainstem bronchial collapse is present in some dogs. There currently is no technique to support collapsed mainstem bronchi; cervical tracheoplasty may not be beneficial if mainstem bronchial collapse is severe.

Figure 1. From: Fossum TW. Small Animal Surgery. St. Louis, MO: Mosby Publishing; 2007
Figure 1. From: Fossum TW. Small Animal Surgery. St. Louis, MO: Mosby Publishing; 2007


The goal of surgery is to support the tracheal cartilages and trachealis muscle while preserving as much of the segmental blood and nerve supply to the trachea as possible. Many techniques have been described. Currently the only techniques that meet this goal are placement of extraluminal individual rings or modified spiral ring prostheses, or intraluminal stents. Generally only the cervical trachea and most proximal portion of the thoracic trachea are supported by extraluminal prostheses even when cervical and thoracic tracheal collapse are present. Intraluminal stent placement involves less risk of interrupting innervation and blood supply but implants are expensive, require fluoroscopic or endoscopic placement, and are associated with serious complications. Currently, intraluminal stents are best used as a salvage procedure for severe, refractory tracheal collapse involving the thoracic trachea. Patients with concurrent laryngeal paralysis or laryngeal collapse may also require arytenoid lateralization or permanent tracheostomy, respectively.


Speaker Information
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Theresa W. Fossum, DVM, MS, PhD, DACVS
Veterinary Medicine & Biomedical Sciences
Texas A&M University
College Station, TX, USA

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