Tracheal Collapse and Stent in a Pomeranian
Gretchen Cawein
Basic Science Advisor: Dr. James Arthur Flanders
Clinical Advisor: Dr. Makoto Asakawa
Senior Seminar Paper
Cornell University College of Veterinary Medicine
March 12th, 2014
Keywords: tracheal collapse, tracheomalacia, tracheal stent, nitinol
Abstract
Acquired tracheal collapse (TC) is a disease that affects predominantly middle-aged toy breed
dogs such as Yorkshire terriers, Chihuahuas and Pomeranians. The pathophysiology of TC is
multifactorial, thus the majority of cases respond to medical and environmental management. In
October of 2013, a case presented to Cornell’s Soft Tissue Surgery Service that had, however,
proven refractory to medical/palliative management. The patient presented with signs that were
virtually diagnostic for TC, and subsequent fluoroscopic and endoscopic imaging supported a
diagnosis of dynamic airway obstruction consistent with grade III tracheal collapse. This case
study will serve to illustrate the etiology, pathophysiology and treatment of this condition. Also
addressed will be the utilization of contemporary imaging modalities, namely interventional
fluoroscopy and endoscopy, to facilitate the re-establishment of patency of the tracheal lumen via
placement of an intraluminal nitinol stent.
Case History and Presentation
The patient was a five year-old spayed Pomeranian who presented to Cornell University
Hospital for Animals for evaluation of moderate-to-severe dyspnea, tachypnea, stertorous airway
sounds and coughing of three years’ duration. Her primary veterinarian first noticed her clinical
signs on a routine physical exam in October of 2010 and, based on her presentation and
signalment, diagnosed her with acquired tracheal collapse. Over the course of three years, the
Pomeranian’s condition was treated with an arsenal of corticosteroids (prednisone, Temaril P)
and antitussives (hydrocodone, Lomotil). However, not only did her condition prove refractory
to pharmaceutical therapy, but her respiratory signs and cough significantly progressed. Upon
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referral to Cornell in October of 2013, it was evident that the dog’s quality of life had rapidly
deteriorated and that conservative management would no longer suffice.
On presentation, the patient was bright but visibly agitated and panting heavily. She was also
hyperthermic (102.6F) and tachycardic (160 beats per minute). Her thorax was virtually
impossible to auscult due to severe referred upper airway sounds, and every successive breath
was associated with a resonant “goose-honk” audible on both inspiration and expiration. The
Pomeranian was morbidly obese (10.5 kg) and bilateral grade III medial patellar luxations were
manifest in a stiff pelvic gait and reluctance to ambulate. The remainder of the patient’s physical
examination was largely unremarkable.
The list of differential diagnoses in a small breed dog with dyspnea or cough includes tracheal
collapse, stenosis, hypoplasia or neoplasia; mitral valve disease; laryngeal paralysis or collapse;
congestive heart failure; pneumonia; small airway disease; allergic or infectious bronchitis;
Dirofilaria immitis and brachycephalic syndrome. The patient’s signalment, history and physical
examination findings were highly suggestive of acquired tracheal collapse. She was admitted to
Cornell’s Soft Tissue Surgery Service to confirm the diagnosis rendered by her primary
veterinarian, to rule out concurrent disease and to assess her eligibility for surgical intervention.
Acquired Tracheal Collapse: Etiology and Pathophysiology
The canine trachea is comprised of an inner mucosa, a fibrocartilaginous middle layer and an
adventitia (in the neck) or serosa (in the thorax) that is supported by a series of C-shaped
cartilaginous rings that open dorsally and are connected by annular ligaments. The dorsal aspect
of this respiratory conduit is spanned by a length of smooth muscle, the trachealis dorsalis, or
tracheal membrane, which serves to regulate variations in diameter in response to intrapleural
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pressure and to allow the trachea to make necessary adjustments in length when the neck is
extended and the diaphragm contracts. In health, the cartilaginous rings of the trachea and larger
bronchi serve to support the structure under negative (extrathoracic) and pleural (intrathoracic)
pressure during respiration, coughing, sneezing, or conditions of increased small airway
resistance.
The precise etiology of acquired tracheal collapse has yet to be evinced. Numerous theories
have been proposed, including inflammatory causes, neurologic deficiency associated with the
tracheal membrane, nutritional and genetic factors. Although TC has been occasionally reported
in large breed dogs, the condition most commonly affects toy and miniature breeds, especially
those who share common physical traits with the chondrodystrophic phenotype (dome-shaped
head, small pointed muzzle and narrow thoracic inlet), which is supportive of a genetic
component in the etiology of the disease1. These dogs also share a predisposition to microscopic
and ultrastructural changes in cartilage associated with chondrodystrophism which are manifest
in a softening of the tracheal rings. Tracheomalacia results from a hypocellularity with respect to
chondrocytes in the cartilaginous makeup of the rings. There is a loss of healthy hyaline cartilage
and replacement with softer fibrocartilaginous or fibrous tissue, as well as a depletion of
chondroitin sulfate and calcium within the remaining cartilaginous matrix. In addition, the
affected tissue becomes dehydrated due to loss of glycoproteins and hydrophilic
glycosaminoglycans, leading to a loss of turgidity.
The result is a loss of structural integrity within the trachea, with concomitant laxity and
prolapse of the dorsal tracheal membrane and subsequent dynamic obstruction of the airway.
This initiates coughing which, with forced respiration, increases intrathoracic pressure, causing
pathological contact between opposing mucosal surfaces within the lumen of the trachea. This
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chronic epithelial injury leads to inflammation, mucous gland hyperplasia causing increased
respiratory secretions, and disruption of mucociliary clearance. These changes lead to further
coughing and the pathological cycle continues.
Medical management is predicated on the idea of intervening at any stage of this process by
identification and management of exogenous triggers and/or concurrent disease combined with
pharmaceutical therapy. Smoke, allergens, dust and excessive heat have all been identified as
contributory factors in this condition. Concurrent infectious or inflammatory pulmonary disease
or heart conditions such as CHF or mitral valve disease have all been implicated as well.
Furthermore, obesity has been shown to exacerbate the condition; extra- and intrathoracic
adipose tissue has significant deleterious effects on the cardiopulmonary system, by the
reduction of thoracic excursions and impingement of lung expansion.
Once all contributory factors have been identified and addressed, antitussives such as
hydrocodone, butorphanol or Lomotil may reduce chronic irritation and damage to the tracheal
epithelium, while corticosteroids such as prednisone or Temaril P are administered to reduce
inflammation. Bronchodilators and antisecretory drugs such as atropine have been used
historically with limited success. Overall, approximately 71% of affected dogs are successfully
treated with medical management2. Others, such as our patient, require surgical intervention to
break the cycle and restore functional patency.
Diagnosis and Assessment
Like many patients with acquired tracheal collapse, the Pomeranian’s basic blood work
parameters were essentially within normal limits 3. Hematology revealed a mild inflammatory
leukogram likely attributable to chronic airway irritation, or tracheobronchitis. Serum chemistry
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analysis showed mild hyperlipidemia as well as mild elevations in creatine kinase and alkaline
phosphatase, attributable to chronic steroid administration.
Although useful in the differential exclusionary process and in the detection of comorbidity,
the diagnostic utility of thoracic and cervical radiographs in cases of suspected TC has come into
question, with sensitivities in the range of 60% reported1. False positives are common as well,
with peritracheal structures such as the esophagus, fat or longus colli commonly mistaken for
tracheal membrane prolapse. Other diagnostic measures such as transtracheal wash and
bronchoalveolar lavage for cytologic analysis may be performed in order to rule out
inflammatory or infectious conditions. However, the dog’s signalment, history and suite of
clinical signs were virtually pathognomonic for acquired tracheal collapse and, in the interest of
expediency and finance, she was taken directly to sedated fluoroscopy.
Fluoroscopy is considered the gold standard for the diagnosis, location and assessment of TC
as, unlike radiography, it allows for continuous appreciation of the dynamics and location of
lesion(s) in real time. In addition, it does not require general anesthesia, which is a consideration
in patients with respiratory compromise. The patient’s study revealed dynamic tracheal collapse
at the level of the caudal cervical trachea; the trachealis dorsalis was notably prominent at the
area of C6 to the thoracic inlet, attenuating the lumen by almost 80% in some phases of
respiration. In addition, the ventral margin of the caudal cervical trachea was noted to flatten and
compress dorsally. However, the intrathoracic trachea was not affected, nor were the mainstem
bronchi.
Once tracheal collapse has been diagnosed and the lesion(s) localized via fluoroscopic
evaluation, tracheobronchoscopy is an invaluable tool in the general assessment of the entire
airway and the extent of collapse. TC is described on a scale of grades I through IV in
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consideration of three factors: the degree of tracheal ring deformation, the integrity of the
tracheal membrane and the percentage of airway occlusion elucidated by endoscopic evaluation.
Grade I represents normal tracheal anatomy with a slightly pendulous tracheal membrane
prolapsing into the lumen with up to 25% decrease in airway diameter. In grade II collapse, the
tracheal rings become less ovoid and more flat, with greater degree of trachealis prolapse and a
50% luminal reduction. Grade III manifests as severe flattening of the cartilaginous rings, with a
tracheal membrane that sags almost to the opposite tracheal wall and a 75% reduction in tracheal
diameter. Finally, grade IV represents total tracheal collapse; the cartilaginous rings are
completely flattened, the trachealis muscle lies on the luminal floor, and the airway is completely obliterated1. Due to the high grade of her collapse (grade III), her moderate age (less than 6
years), the absence of comorbidities, acceptable anesthesia status and poor response to medical
management, the Pomeranian was deemed an appropriate candidate for the establishment of a
patent airway via the placement of an intraluminal nitinol stent.
Nitinol Stent
The nitinol stent is a relatively new addition to the surgical options traditionally utilized to
address TC. Until approximately a decade ago, the most popular method was the placement of
extraluminal prostheses, either in the form of individual rings or as a continuous spiral. Although
still an option, particularly in cases of extrathoracic TC, extraluminal prostheses have been
associated with a number of complications, particularly laryngeal paralysis. The paralysis is
attributed to damage to the recurrent laryngeal nerve during surgical manipulation or as a result
of long-term contact or rubbing against the prosthetic device2. Often this condition necessitates
at least unilateral arytenoid lateralization, with its own set of potential complications.
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Endotracheal stenting has the advantage of being minimally invasive, with no potential
damage to the tracheal blood supply or the recurrent laryngeal nerve. It also requires shorter
anesthesia time, while providing an immediate reduction of clinical signs upon recovery.
Procedure
Nitinol is a nickel-titanium alloy that is deformable under cool temperatures. The woven
mesh stent is compressed into the delivery system and, once deployed, expands to and maintains
its original volume at body heat. The area of tracheal collapse is located and assessed under
sedated fluoroscopy, with anatomic landmarks used to record the cranial- and caudalmost extent
of the collapse. Under general anesthesia, the maximal tracheal diameter is then determined
under 20 cm H2O of pressure by the insertion of an esophageal marking catheter that runs
alongside the area of interest. Each grade on the catheter represents 10 mm, which allows for
extrapolation of the diameter of the airway while accounting for radiographic magnification. The
stent size is calculated as 10-20% over the maximal tracheal diameter4. The stent sits over a
metal cannula. With the patient in lateral recumbency and positioned such that the intrathoracic
and cervical portions of the trachea lie in a straight line, the entire device is advanced to the
desired position within the trachea, the stent is unsheathed and the cannula is simultaneously
retracted, leaving the stent behind. Ideal placement extends at least one centimeter beyond the
cranial and caudal margins of the collapse to allow for any incidence of shortening over time.
Orthogonal radiographs are then obtained to verify position. In this patient, the lesion was
located to the area of C6 to the thoracic inlet. A 77 x 12 mm nitinol stent was placed
approximately 3 centimeters cranial and 4 centimeters caudal to the margins of the affected area
without complication.
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Post-Procedural Care
The patient recovered smoothly and uneventfully from anesthesia and was placed in 40%
ambient oxygen. Post-procedural vital parameters were within normal limits, with a notable 75%
reduction in respiratory rate, normal bronchovesicular sounds on auscultation and an apparent
resolution of the previously-noted respiratory “goose honk”. She was administered a single dose
of dexamethasone SP and maintained on fluids and tapering intravenous butorphanol throughout
the night. Oxygen saturation values were reportedly unobtainable, but she rested comfortably in
the intensive care unit, with no evidence of respiratory distress.
The following day, the dog was weaned off oxygen supplementation and breathed easily
unassisted. Her intravenous antitussive was also tapered off in anticipation of discharge the
following day. However, she was experiencing mild episodes of regurgitation and so was
detained in the hospital an additional day for observation as well as antiemetic and
gastroprotectant therapy. Our patient was discharged with a tapering anti-inflammatory regimen
of oral prednisone, hydrocodone and a gastroprotectant, as well as nutritional recommendations
for weight loss. Her owners were also advised against neck leads, to limit her exposure to
environmental stressors such as high heat and humidity, smoke, perfumes, air fresheners and
inhaled allergens, and to schedule post-procedural thoracic radiographs in one month and every
three to four months thereafter.
Prognosis
Short term complications of intraluminal tracheal stenting are rare, while long-term
complications are most commonly associated with technical errors in stent selection and
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placement. These may include stent fracture and migration, exuberant granulation at the cranial
and caudal stent margins, diminished mucociliary clearance and stent shortening5. As postprocedural morbidity is largely associated with coughing, the judicious administration of
antitussives is an important component of convalescent therapy. In addition, frequent and
aggressive reevaluation (i.e. thoracocervical radiography) is recommended for the duration of the
patient’s life such that complications may be detected prior to clinical sequelae. Stent fracture is
addressed by emergent restenting6 to avoid propagation of the fracture, whereas high-dose
corticosteroids are effective against excessive inflammation. The use of nitinol has reduced the
incidence of stent shortening but when it does occur, a second stent may be placed or
extraluminal rings may be applied in areas of persistent collapse.
Although a relatively large number of tracheal stents have been placed in dogs over the last
decade, there are actually very few studies and case reports published on the long-term outcomes
of these patients. One study cites immediate improvement in clinical signs at 95.8 % (23/24
dogs), with an acute mortality rate of 8.3% (2/24) within three to nine days of placement (due to
either incorrect placement or subcutaneous emphysema [suspected secondary to tracheal
tearing])7. Ettinger anecdotally reports intraluminal stents that have remained in place without
complication for six to seven years, with periprocedural morbidity and mortality rates of less
than 5% and less than 2%, respectively8. All-in-all, placement of the nitinol stent as a therapy
for tracheal collapse is associated with an overall fair to good outcome9.
Conclusion
At one month subsequent to the procedure, the patient’s primary veterinarian reported full
resolution of dyspnea and normalization of vital parameters, albeit with a persistent cough that
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was responsive to hydrocodone. A lateral thoracic radiograph at that time revealed full patency
of the tracheal lumen, with no evidence of stent fracture, migration or shortening. At four
months, the Pomeranian’s owners reported resolution of all clinical signs other than occasional
episodes of coughing which were treated with hydrocodone as needed. They also reported a
marked increase in energy and playfulness, improved exercise tolerance, a weight loss of over
two kilograms, and an overall improvement in our patient’s quality of life.
References
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Cats. St. Louis: Saunders Elsevier.
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