Tracheal collapse is a severely debilitating disease which can lead to absolute airway obstruction and death if not controlled. Over the years, a number of management techniques have been described, ranging from medication alone, to surgery on the trachea, the use of extraluminal supports and, lately, intraluminal stenting. The diversity of described techniques suggests that we have not yet managed to develop an ideal strategy for treating this difficult condition.
Tracheal collapse is a progressive chronic condition of the trachea that appears to be irreversible. The clinical signs associated with tracheal collapse are
Harsh dry goose honk cough
Coughing when picked up or especially if someone pulls on their collar
Cyanosis and potential collapse with excitement
Marked wheezing on inspiration
The precise aetiology of tracheal collapse has long been a subject of controversy. The frequent incidence of signs in dogs aged six months or less lends support to the suggestion that the underlying cartilaginous abnormality has a congenital origin. Conversely, the progressive onset of signs later in life in other dogs appears to indicate an acquired aetiology. A third alternative, consistent with both of the above, is that the functional tendency to collapse is indeed congenital, but other secondary or 'initiating' factors are necessary before the condition becomes symptomatic. Factors previously incriminated in precipitating the symptomatic state include inhalation of irritating substances, such as allergens or pollutants, congestive heart failure, excessive barking, and obesity The implication of an initiating factor in more than half of the cases in one series confirms the theory of a primary, congenital defect which only gives rise to a clinically significant condition in the presence of other factors.
Treatment of tracheal collapse is focused on palliation of clinical signs, initially using medical therapy; but this may not in all cases resolve clinical signs in the long term. If conservative therapy fails, reported treatment options include use of tracheal ligament plication, extraluminal prosthetic rings or endoluminal tracheal stents.
Classification of Collapsing Trachea
Grade I - tracheal membrane is slightly pendulous, cartilage maintains normal shape, lumen reduced approximately 25%
Grade II - tracheal membrane widened and pendulous, cartilage is partially flattened, lumen reduced approximately 50%
Grade III - tracheal membrane is almost in contact with dorsal trachea, cartilage is nearly flat, lumen is reduced approximately 75%
Grade IV - tracheal membrane is lying on dorsal cartilage, cartilage is flattened and may invert, lumen is essentially closed
The current gold standard for establishing a diagnosis is tracheoscopy, as this allows the collapse to be directly visualised and graded from I to IV. Plain radiography is unreliable and may miss up to 60% of cases. Radiography can be valuable and the length of collapse can be identified in a fully awake animal using real-time fluoroscopy. In addition, if coughing is induced, the extreme airway pressures generated will usually reveal more extensive collapse than identified during relaxed breathing. Anatomical landmarks are identified to record the cranial-most and caudal-most extent of the collapse. In addition, mainstem bronchial collapse can be identified during fluoroscopy and should be noted when present. If fluoroscopy is not available, the extent of the collapse can be assessed using inflated views in the anaesthetized patient. Care must be taken in anaesthetizing these patients, as recovery can be problematic. A measuring catheter is placed within the esophagus to allow for radiographic magnification. The endotracheal tube is withdrawn until the distal-most aspect just beyond the larynx and the cuff is gently inflated. Positive pressure ventilation of 20 cm H2O is temporarily performed to achieve maximal tracheal expansion as a radiograph is taken. This will show the extent of the collapsing segment. Paradoxically, this section will 'over inflate'. The radio-opaque marks on the catheter are used to determine the radiographic magnification that is then used to extrapolate the actual maximal diameters of both the intrathoracic and cervical trachea. It is important to note maximal measurements of both the cervical and intrathoracic trachea, as these measurements can vary.
A rational approach would lie in the elimination of factors which initiate the symptomatic state and in the suppression of the self-perpetuating cycle of cough, mucosal pathology and failure of the mucociliary escalator. Antiinflammatory agents have been widely recommended as a means of interrupting the cycle of tracheal inflammation and cough. The identification of dogs with an apparently allergic component to their clinical signs suggests that their immunosuppressive activity may be an additional factor in the reported efficacy of steroids for this condition. It seems unlikely, however, that the more advanced proliferative changes in the tracheal mucosa can be reversed by steroidal therapy and the potential side effects (e.g., obesity, hyperpnoea, weakening the cartilage) may mitigate against their prolonged use. The long-term use of steroids in the management of tracheal collapse is unwise with the exception of those cases in which an allergic aetiology has been established.
Medical therapy is recommended for all animals with mild clinical signs and for those with less than 50% collapse, because it results in improvement in clinical signs in most dogs. Weight loss is critical to the success of other medical therapies. Environmental modifications, such as use of a harness instead of a collar and the creation of a nonsmoking atmosphere, may help some dogs, as will management of concurrent underlying conditions.
Medical therapy for dogs with tracheal collapse includes antitussives, antibiotics, bronchodilators and/or antiinflammatory agents (NSAIDs). Sedation with acepromazine and/or diazepam and supplemental oxygen may be required in severely dyspnoeic patients. Paediatric metered dose inhalers used with spacers and face masks may be used in cooperative dogs to administer aerosolized bronchodilators and corticosteroids. Mucolytics and saline nebulization may benefit those with excess mucus production and infection.
This is procedure that had fallen out of favour in recent years with the advent of intraluminal stenting procedures. Recent work suggest that this is still a viable option for severe cases of tracheal collapse. The concern has always centred on the fact that it is only possible to successfully place prostheses on the cervical trachea, with the concern being that the intrathoracic trachea would continue to collapse.
The trachea reinforced by suturing the trachea to four to six polypropylene rings around it. The rings (approximately 5 mm wide) are made from polypropylene syringe holder with four to six holes drilled for suture placement. A ventral midline skin incision is made from the larynx to the thoracic inlet. The subcutaneous tissue and sternohyoideus muscles are separated to expose the trachea. The thyroid arteries and recurrent laryngeal nerves are bluntly dissected from the trachea only in the area of ring placement, and a polypropylene ring is placed between the tracheal wall and the recurrent laryngeal nerves; this is sutured to the tracheal cartilages and the trachealis muscle with 3-0 polypropylene.
Recent work indicates that survival time postsurgery is excellent and that the presence of intrathoracic tracheal collapse does not prevent this procedure being carried out. Some dogs may require continued medical support.
Clinical improvement rates in 75%–90% of animals treated with self-expanding, intraluminal stents have been reported. Tracheal stents are best reserved for dogs with tracheal collapse that are not good candidates for extraluminal prostheses and have failed medical therapy. They have the advantage in that they can be placed in dogs with intrathoracic tracheal collapse. The main contraindication to their use is in dogs with collapse of the main stem bronchii. They offer the advantages of a minimally invasive procedure with a short postoperative convalescence, and rapid restoration of airway lumen.
Postoperative coughing is never totally reduced, as the stent interferes with the mucociliary clearance. The stent is prone to kinking, and the tracheal wall is prone to granuloma formation at the rostral and caudal extents of the stent. Additionally, these stents are very difficult to remove after deployment, and adjustment of a broken unit is not possible.
Owners must be advised that tracheal stents should be deployed as late in the animals' life as possible, since few patients live more than 2–3 years without developing one of the previously mentioned significant complications. Unfortunately, medical therapy, surgery, or stenting are not cures for tracheal collapse. When used appropriately in the proper patients, however, stenting can significantly improve the patient's quality of life when medications alone are no longer adequate. It is the author's experience that granulation tissue is common after 6 months, and steroids are required to try and minimize this problem.
We do not have an ideal solution for this condition as yet. If medical management fails to control, then consider surgery or stent placement. Does the future lie in using three-dimensionally printed tracheal supports or grafts?