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Use of a nitinol wire stent for management of severe tracheal stenosis in an eclectus parrot (Eclectus roratus).

Abstract: A 25-year-old, female eclectus parrot (Eclectus roratus) presented for dyspnea 3 weeks after anesthesia and surgery for egg yolk coelomitis. Radiography, computed tomography, and tracheoscopy revealed multiple tracheal strictures spanning a length of 2.6 cm in the mid to distal trachea. Histopathologic examination revealed mild fibrosis, inflammation, and hyperplasia consistent with acquired tracheal strictures. Tracheal resection was not considered possible because of the length of the affected trachea. The strictures were resected endoscopically, and repeated balloon dilation under fluoroscopic guidance over the course of 10 months resulted in immediate but unsustained improvement. Computed tomography was used to measure the stenotic area. A 4 X 36-mm, custom-made, nitinol wire stent was inserted into the trachea under fluoroscopic guidance. After stent placement, intermittent episodes of mild to moderate dyspnea continued, and these responded to nebulization with a combination of saline, acetylcysteine, and dexamethasone. Multiple attempts to wean the patient off nebulization therapy and to switch to a corticosteroid-free combination were unsuccessful. The parrot eventually developed complications, was euthanatized, and necropsy was performed. Histologically, the tracheal mucosa had widespread erosion to ulceration, with accumulation of intraluminal exudate and bacteria, severe degeneration of skeletal muscle and tracheal rings, prominent fibrosis, and mild to moderate, submucosal inflammation. Clinicopathologic findings in this case suggested tracheomalacia, which has not been previously described in birds. Custom-made tracheal stents can be used for severe tracheal stenosis in birds when tracheal resection and anastomosis is not possible. Complications of tracheal stent placement in birds may include tracheitis and tracheomalacia. To our knowledge, this is the first report of tracheal stent placement in an avian species.

Key words: tracheal stenosis, tracheomalacia, dyspnea, anesthesia, nitinol wire stent, balloon dilation, intubation, avian, eclectus parrot, Eclectus roratus

Clinical Report

A 25-year-old, female eclectus parrot (Eclectus roratus) was referred for examination because of respiratory distress. Three weeks before presentation, the bird had been anesthetized and intubated at the primary avian specialty clinic for surgery to correct egg yolk coelomitis (day 0). Despite initial recovery, the bird developed mild stridor. On day 3 after surgery, and by day 21, signs progressed to severe dyspnea, open mouth breathing, and 11% loss in body weight from 428 g to 382 g. The bird additionally had a chronic history of feather picking. Husbandry was acceptable, and there were no recent changes in environment or diet. The owners reported no history of exposure to smoke, fumes, or other airborne toxins. This bird was part of a multibird household, but no other birds exhibited similar clinical signs. Results of physical examination demonstrated increased referred lung sounds with no wheezes or crackles appreciated on auscultation. Respiratory signs improved, but did not abate completely, with oxygen therapy. Based on the temporal association with prior intubation and the presenting signs, tracheal obstruction was the primary concern.

The bird was anesthetized with sevoflurane in oxygen delivered by facemask and a nonbreathing system. A rapid assessment of the trachea was performed with a portable 1.9-mm, semirigid fiberscope (MDS Incorporated, Valrico, FL, USA), confirming the presence of several tracheal strictures. The bird was intubated with a 3.0-mm, uncuffed endotracheal tube and a 4.5-mm air sac cannula was placed in the left caudal thoracic air sac and secured with 4-0 nylon monofilament suture (Ethicon, San Angelo, TX, USA). After this procedure, the patient stabilized and was referred to the Zoological Medicine Service, University of Georgia (Athens, GA, USA) on day 22 for further evaluation. On initial examination, the bird was anesthetized for blood sampling and radiographs, and the air sac cannula was removed. Results of routine hematologic testing and plasma biochemical analysis were unremarkable. (1) Fecal samples were collected, and no parasites were seen on fecal flotation or direct microscopy. On survey orthogonal whole-body radiographs, multifocal, ill-defined, soft tissue structures protruded into the tracheal lumen from the dorsal and ventral walls. These were located in the mid- and distal trachea (Fig 1). A well-defined, curvilinear, soft tissue structure was also identified in the caudoventral coelom. Based on the location of this structure, airsacculitis was suspected. Because of the identification of the multiple strictures affecting at least a 2.6-cm length of the trachea and the degree of tracheal luminal narrowing, endoscopic debridement and balloon dilation was pursued on day 23.

For tracheal dilation, the bird was premedicated with butorphanol (1 mg/kg IM), and anesthetic induction was achieved using 5% isoflurane in oxygen delivered at 1 L/min by face mask. A 3.0-mm, uncuffed endotracheal tube was used for intubation, and anesthesia was maintained with isoflurane adjusted to individual patient requirements. The left caudal thoracic air sac was cannulated with a 3.0-mm, uncuffed, sterile endotracheal tube, and anesthesia was maintained via the cannula connected to a small-animal ventilator (Vetronics Bioanalytical Systems Inc, Lafayette, IN, USA). A 22-gauge, 1.5-inch spinal needle was placed in the right distal ulna for intraosseous constant-rate infusion of crystalloid fluids (lactated Ringer's solution, 10 mL/kg per hour intraosseous [10]). Tracheoscopy was performed with a 1.9-mm rigid telescope with integrated sheath (Karl Storz Veterinary Endoscopy, Goleta, CA, USA) and revealed at least 3 strictures spanning the distal one-third of the trachea (Fig 2). A horizontal, longitudinal band of fibrous tissue connected the second and third strictures. This band was resected with a 1-mm (3 Fr) forceps (Karl Storz Veterinary Endoscopy) passed though a working channel, which was followed by fluoroscope-guided dilation with a 4-mm X 4-cm, biliary, balloon-dilation catheter (Hurricane biliary dilatation catheter, Boston Scientific Corp. Boston, MA, USA). This balloon catheter has a nominal diameter of 1.9 mm and a total working length of 180 cm. The balloon section was 2 cm long, with a maximal diameter of 4 mm. The balloon was positioned and inflated 3 times to 30 pounds per square inch (psi) (2 atmosphere units) and held in position for 1 minute, per the manufacturer's instructions. Histologic evaluation of the tissue removed showed mild fibrosis, histiocytic and heterophilic inflammation, and epithelial hyperplasia, consistent with a diagnosis of tracheal stricture. The bird was intratracheally intubated, and the caudal thoracic air sac cannula was removed for coelioscopic evaluation. Extensive, but sterile, yolk-associated coelomitis was confirmed visually and by results of histopathologic and microbiologic testing.

Because of expected postoperative inflammation of the trachea and the need to provide intratracheal medication, the air sac cannula was replaced before anesthetic recovery. Dexamethasone sodium phosphate (0.5 mg/kg) was administered intratracheally after the tracheoscopy and was repeated once daily for 7 days. The dose was then decreased stepwise over 2 days (0.125 mg/kg x 1 day, then 0.06 mg/kg x 1 day). The treatment protocol consisted of orbifloxacin (30 mg/kg PO q12h X 16 days), meloxicam (0.5 mg/kg PO q12h x 24 days), itraconazole (10 mg/kg PO q24h x 16 days), and amphotericin B (5 mg/mL in 5% dextrose nebulized for 20 minutes q12h X 7 days).

On day 27, tracheoscopic examination revealed mild inflammation but no evidence of decreased lumen size or infection. Coelomic endoscopic examination via the right caudal air sac showed mild, diffuse, yolk-associated coelomitis. On day 30, tracheoscopy showed minor focal areas of inflammation without evidence of recurrent stenosis or infection. However, clinical signs recurred, and tracheal balloon dilation inflated 3 times at 30 psi and medical treatments described above were repeated on days 40, 63, 74, 91, 110, 256, and 329. Dyspnea temporarily resolved for varying periods of time after each procedure but always recurred; at which point, distal strictures were again documented by tracheoscopy. Because the clinical signs recurred with repeated balloon dilation procedures, other treatment options were investigated, including the placement of an intraluminal tracheal stent similar to that described in dogs. (2) Computed tomography (CT) images were obtained to accurately measure the strictured areas of the tracheal lumen as well as the maximum diameter of the healthy trachea cranial and caudal to these areas. The strictured area was easily distinguished, particularly on dorsal plane reconstructions, and was characterized by generalized thickening of the tracheal rings circumferentially. Increased mineral was seen in this area, which was interpreted to be caused by enlargement of the tracheal rings or mineralization of adjacent soft tissues in between the tracheal rings. In the caudal area of the tracheal ring narrowing, a luminal stenosis that was associated with a focal eccentric band of soft tissue was visible. Based on CT images, the narrowed length of the trachea measured 2.6 cm, and the total length of the trachea was 10.2 cm from the larynx to the syrinx; therefore, 25% of the trachea was affected. The healthy tracheal diameter was 3.8 mm cranial and 4.9 mm caudal to the narrowing, respectively. The severity of narrowing ranged between 1.4 mm and 2.8 nun of minimal, luminal diameter. The most severe narrowing was located at the caudal end of the affected trachea (Fig 3), which was 1.1 cm cranial to the syrinx.

Based on the measurements obtained from the CT images, a 4-mm X 36-mm, custom-made nitinol wire stent was chosen to address the stricture in the trachea. This customized stent was manufactured to be 10% oversized, self-expanding, and equivalent to the maximum diameter of the healthy-appearing areas of trachea cranial and caudal to the strictured area. Preoperative hematologic results on day 375 revealed leukocytosis (32 800 cells/[micro]L; reference interval, 13 700 [+ or -] 6 300 cells/ [micro]L (1)). On day 376, the bird was anesthetized with an air sac cannula as previously described. Endoscopic examination was performed to confirm the cranial and caudal extent of the tracheal narrowing and stricture. The custom-made stent (Vet Stent, Infiniti Medical, Menlo Park, CA, USA) was introduced through the glottis and advanced under fluoroscopic guidance. The un-deployed stent was positioned just cranial to the opening of the syrinx. Once fully deployed, the stent spanned the cervical trachea between the cranial endplate of the seventh cervical vertebra and the syringeal opening. At the end of the deployment, most of the stent was fully expanded; the area of submaximal stent expansion corresponded to the most affected area of the trachea. This area, measuring 0.4 cm long, was seen approximately 0.8 cm from the distal aspect of the stent.

The bird was treated with the same medical protocol as mentioned previously with systemic antibiotics, antifungal drugs, and anti-inflammatory medications. Ancillary nutraceuticals consisted of Imuno-2865 (3-5) (one-quarter capsule PO q24h; Animal Necessity, LLC, New York, NY, USA) and Bird Bene-Bac (0.5 g PO q24h; PetAg Inc, Hampshire, IL, USA). On day 385, 9 days after the stent was placed, results of clinicopathologic testing were unremarkable. (1) Tracheoscopy revealed minimal inflammation, no evidence of infection, and little mucus accumulation (Fig 4). Radiographs indicated no change in stent position or in tracheal diameter cranial to, at, or caudal to the stent (Fig 5). Specifically, the submaximally distended area was unchanged, with no increased soft tissue seen in the tracheal wall or lumen. The bird was discharged from the hospital.

On day 393, the bird was presented because of respiratory difficulty, 17 days after initial stent placement. The bird was hospitalized for 4 days, and repeat tracheoscopy revealed partial occlusion with tissue growth over the stent wires at the distal extent. Various nebulization recipes were tried (eg, sterile saline only, a saline/acetylcysteine [20 mg/ mL] combination, and a saline/acetylcysteine [20 mg/mL]/dexamethasone sodium phosphate [0.16 mg/mL] combination). Nebulization with saline, acetylcysteine, and aminophylline (1.85 mg/mL) was used for the next 4 days, but treatment did not yield any improvement. On day 401, nebulization with saline, acetylcysteine, and dexamethasone sodium phosphate was initiated. The risks of steroid-induced immunosuppression were explained to the client. Amikacin (5 mg/mL) and terbinafine (0.625 mg/mL) were added to this mixture as a prophylactic to infection. During acute episodes, this stock solution was used at full strength, 5 [cm.sup.3] nebulized q12h. However, for maintenance, the client usually diluted the stock solution 1:4 or 2:3 with sterile saline and nebulized the bird q12h to q48h as needed. Multiple attempts to wean the bird off nebulization therapy and to switch to a steroid-free combination were unsuccessful.

On day 716, tracheoscopy and radiographs were repeated and revealed persistent improvement in airway diameter (Fig 4) and no change in stent position. After stent placement, intermittent episodes of mild to moderate increased respiratory effort, often accompanied by stridor and stertor, continued to occur. These episodes usually responded well to nebulization (dexamethasone sodium phosphate, saline, acetylcysteine), although treatment sometimes also included meloxicam (0.3 mg/kg PO q24h X 5 days) alone or with an antibiotic (enrofloxacin [25 mg/kg PO q24h X 10 days], amoxicillin, and clavulanate potassium [125 mg/kg PO q24h X 10 days], sulfamethoxazole/trimethoprim [100 mg/kg PO q12h X 14 days], or ciprofloxacin [20 mg/kg PO q12h X 10 days]).

On day 1043, the bird was presented for dyspnea of several days' duration that did not respond to nebulization and medical therapy. Repeat radiographs on day 1058 revealed prior stent foreshortening and demineralization of the tracheal rings 0.8 cm cranial to and overlying the cranial half of the stent. Tracheoscopy revealed thick, yellowish, mucoid exudate lining the trachea cranial to the stent and extending down the tracheal wall. Just cranial to the stent, the trachea appeared to be eroded, and on inspiration/expiration, ballooning of the tracheal wall was visible. Results of cytologic examination and bacterial culture of tracheal swab samples were unremarkable. The parrot continued to experience intermittent dyspnea that responded poorly to nebulization and medical therapy until day 1108, when the patient presented for severe dyspnea. Tracheoscopy revealed 2 areas of severe, partial (>50%) obstruction of the trachea by what appeared to be inflammatory debris, and euthanasia was elected.

At necropsy, gross examination of the trachea revealed a loss of rigidity just cranial to the stent. Upon opening the trachea, multiple, yellow to tan, nodular to plaque-like aggregates of thick, caseous necrotic material were observed adhering to the mucosal surface and filling >50% of the lumen at their respective sites (Fig 6). Histologically, none of the trachea was normal, although changes in the proximal trachea were less severe than changes in or adjacent to the stented trachea. Throughout the trachea, there was partial to complete loss of tracheal rings with expansion and replacement with fibrous tissue, most of which was ossified. (Fig 7). External skeletal muscle was also mildly to markedly thinned and sometimes absent, with scattered, individual myofiber necrosis, and in one section, just proximal to the stent, a focal area of herniation of the very thin muscle layer was present between 2 degenerate segments of bone into the submucosa (Fig 8). The submucosa was diffusely expanded by abundant fibrous tissue, with mild to occasionally moderate mucosal and submucosal inflammation that surrounded irregular fragments of bone and cartilage. Inflammation was primarily heterophilic and lymphoplasmacytic. with few granulomatous foci. Mucosal epithelium was typically severely eroded to ulcerated, although rare foci of normal to hyperplastic epithelium were observed in the proximal trachea. Multifocally, the tracheal lumen contained aggregates of abundant necrotic debris mixed with degranulated heterophils, numerous mixed bacteria including mats of gram-negative, filamentous bacilli, few fungi, and fragments of bone. Ovoid clear spaces, interpreted to represent the location of the stent wires, were observed in the submucosa, between fragments of bone, and between striated myofibers. The histopathologic evidence of marked loss of the cartilaginous or ossified tracheal rings in conjunction with the gross finding of decreased tracheal rigidity adjacent to the stent and recurring episodes of dyspnea are consistent with tracheomalacia.


In this parrot, tracheal stent placement was considered successful, based on improved case medical management, which did not require repeated anesthesia and surgery over the subsequent 22 months. Before stent placement, conservative management including ballooning produced only temporary improvement. Long-term nebulization and medical therapy with stent placement was needed to decrease respiratory clinical signs. Ultimately, unresolving tracheitis, deciliation, and tracheomalacia led to euthanasia. To our knowledge, this is the first report of successful management of severe tracheal stenosis using a tracheal stent in an avian species. In this case, radiographic and endoscopic imaging 22 months after stent implantation did not indicate stent fracture or intraluminal narrowing.

Unlike mammals, the avian trachea is composed of closely spaced, complete tracheal rings with no musculus trachealis. (6) The typical avian trachea is 2.7 times longer and 1.3 times wider than that of a comparative mammal. (6) The resultant tracheal dead space is 4.5 times greater than a comparably sized, mammalian trachea. The avian species can compensate for the difference with a low respiratory frequency (one-third that of mammals) and an increased tidal volume (4 times that of mammals). (6) The diameter of the tracheal cartilage narrows abruptly caudally in some species. (7) Uncuffed endotracheal tubes with a smaller internal diameter (IO)/outer diameter (OD) should be used. Because tubes can have different OD for the same ID, the ID/OD sizes should be verified and recorded. (7) Depending on the size of the animal, a smaller tube diameter and length is recommended to prevent iatrogenic trauma to the tracheal lining caudal to the glottis. (6) If a shorter tube is used, care must be taken to decrease the risk of aspiration around the uncuffed endotracheal tube, and adjustments to anesthetic flow must be considered. (7) Cole endotracheal tubes create an effective seal and do not extend as far down the trachea; however, they have an increased resistance to airflow and a higher risk of occlusion by a tracheal mucous plug. (7) During avian intubation, the glottis should be visualized, and the head should be extended and aligned with the neck to maintain a straight trachea and central placement of the distal end of the tube into the tracheal lumen. (7) Copious, thick mucus production can be seen during inhalant anesthesia because of the drying effects of the inspired cold, dry gasses. (7) The bevel tip on certain endotracheal tubes may cause focal irritation, and any movement of the tube can cause damage to the trachea, resulting in proliferation of granulation tissue and fibrosis. (7) All anesthetic equipment attached to the endotracheal tube should be carefully disconnected when repositioning the bird because this equipment may weigh more than the patient. Care should be taken to wash tubes thoroughly to ensure that all disinfectants have been removed, and the tubes should be completely dry before use. In animals with preexisting tracheal disease, caution should be taken when placing an endotracheal tube, and an air sac cannula should be considered.

Tracheal diseases include infectious (bacterial, mycobacterial, fungal, parasitic, and viral), foreign body, neoplastic, granulomatous, extramural compressive, and traumatic conditions, including strictures secondary to intubation damage. (7) Birds have a similar clinical presentation regardless of the inciting cause. They may exhibit stridor, dyspnea, vocalization changes, open mouth breathing, and tail bobbing. (7) Acute onset of these clinical signs is often associated with tracheal obstruction. (7) Most birds lack the dorsal muscular portion of the mammalian trachea, making the avian trachea less expandable. Dyspnea will occur quicker in birds, despite less-severe narrowing compared with mammals, in which dyspnea at rest is only noticed when the tracheal lumen diameter is reduced by 85% to 90%. (8) Radiography, tracheoscopy, and CT are considered useful diagnostic tools.

Tracheal stenosis can be managed conservatively or surgically. (7) Types of surgical management considered in the present case consisted of tracheal resection and anastomosis, and conservative management included ballooning with subsequent medical treatment and tracheal lumen stent placement. In cases of tracheal obstruction, placing an air sac cannula often results in a dramatic improvement in clinical signs. Conservative management in this case provided only temporary benefit. The use of steroids in birds is controversial, causing immunosuppressive effects that are more severe than in mammals, and use may result in fungal infection of the respiratory tract. (7,9) We preferred using nonsteroidal anti-inflammatory treatment; however, ultimately the referring veterinarian and client found that nebulization with steroids was the only treatment that provided clinical improvement.

Balloon dilation in birds may lead to iatrogenic damage because of the presence of complete tracheal rings. (7) Balloon dilation must be done multiple times to be effective in humans. (7) In this case, repeated balloon dilation was only effective in providing temporary improvement. Successful tracheal resection and anastomosis have been reported in the hybrid goose (Ariser species), bald eagle (Haliaeetus leucocephalus), mallard duck (Anas platyrhynchos), and blue and gold macaw (Ara ararauna) 12 The longest total tracheal segment resected consisted of 15 tracheal rings in a blue and gold macaw. (8) An ostrich (Struthio camelus) was reported with tracheal collapse and was successfully treated with a tracheal split-ring prosthesis placed at surgery. (13) In our case, the length of affected trachea was 2.8 cm and involved 26 tracheal rings; therefore, we concluded that tracheal resection was not a viable option and intraluminal location of the lesion made external support impossible.

In dogs, surgical management is the main approach for treatment of tracheal collapse refractory to medical treatment. (2,14) Different forms of endotracheal stenting have been attempted. (2) Studies report initial survival rates of 92% for endotracheal stenting and 94% for surgical management. (2) Long-term results after stenting in dogs have been favorable, with 33% remaining asymptomatic, 61% markedly improved, and only 6% remaining symptomatic. (2) Two canine case reports of tracheal collapse were treated with nitinol stents and were eventually successfully managed; however, complications, such as stent migration, stent fracture, and pneumonia, were reported. (2,15) Another study evaluated placement of self-expandable, nitinol intratracheal stents in 4 dogs and determined that these stents provide adequate stability of the trachea. When placed from the midcervical to the thoracic trachea, stenting increased the diameter of the entire cervical to thoracic tracheal area. (16) Three cats received intraluminal tracheal stents for either benign or malignant tracheal obstruction, and results showed that stenting was easily, safely, and rapidly performed without complications and resulted in immediate improvement in clinical signs. (17)

The ideal tracheal stent would have the following properties: 1) easy, precise implantation; 2) airway patency without migration because of sufficient radial force; 3) high elasticity without material fatigue; 4) longitudinal flexibility for tolerance without airway damage; 5) easy removal if indicated; 6) minimal interference with mucociliary clearance; and 7) lack of associated granulation tissue formation, foreign body reaction, or infection. (2) Currently, no stents meet all these requirements. Tracheal stents are generally made of silicone, plastic, metal, or hybrids that combine different materials. (2) Because of the large area of trachea affected in this parrot, a 4 x 36-mm, custom-made, nitinol, intraluminal wire stent was placed. This type of stent is durable, exhibits excellent flexibility allowing adaptation to the local anatomy, can be repositioned before complete deployment, and has atraumatic stent ends that minimize mucosal trauma and inflammatory response. (18)

In humans, long-term complications associated with the placement of uncovered stents for benign strictures are relatively high, and covered and/or removable stents are usually elected when used for benign stricture in mucosally lined, luminal structures. (19) Other complications of stent placement are obstructive granulation tissue, stenosis at the ends of the stent (epithelium growing over stent wires), migration of the stent, mucous plugging, infection, and stent fracture. (19) Although not observed in this case, potential for stent fracture is present where range of motion of the neck is likely to be greater than for a human or even a dog, with subsequent stresses on the stent. Complications in this case were chronic, intermittent dyspnea after stent placement; subsequent severe, ulcerative tracheitis with intraluminal accumulation of fibrinonecrotic debris and bacterial mats; and atrophy of the tracheal rings and skeletal muscle throughout the area where the stent was placed, as well as in the adjacent trachea. Although the latter complications were unforeseen, long-term corticosteroid administration may have predisposed this patient to tracheitis. Although corticosteroids are generally contraindicated in birds, they were used in this case because the patient exhibited respiratory signs when they were discontinued, usually within several days. Because bacterial and fungal infections were possible complications, corticosteroids were only used at the lowest effective dose and interval possible.

Clinicopathologic findings in this case suggest tracheomalacia, which has not been previously described in birds. In humans, tracheomalacia is associated with weakness of the tracheal walls because of softening of the supporting cartilage and hypotonia of the myoelastic elements. (20) These patients have a tracheal cartilage to soft tissue ratio as low as 2:1, whereas the reference interval is approximately 4.5:1. (20) Some of the causes of this disease are chronic airway and soft tissue inflammation (chronic obstructive pulmonary disease, asthma); chronic irritation of the airway (smokers, environmental pollutants); malignancy (intraluminal or extraluminal tumors); long-term, positive-pressure ventilation; and endotracheal intubation. (20)

Because the bird's respiratory signs appeared to begin after the first anesthetic surgical episode, this intubation may have started the cascade that resulted in tracheomalacia. Recurring intubations could also have contributed to deciliation and unresolving or relapsing tracheitis. Unfortunately, in this case, medical therapy alone did not resolve the chronic dyspneic episodes, and balloon dilation and ultimately stent placement were needed for the patient's survival. Ultimately, chronic inflammation with fibrosis and loss of cilia, steroid use, and biomechanics likely had a role in the bird's demise. Significant biomechanical differences exist in birds compared with mammals, including increased range of motion of the neck, increased tracheal flexibility, comparatively less muscle and soft tissue surrounding the trachea, and complete tracheal rings. The stent used in this case, although flexible, was more rigid than the trachea itself, particularly once the tracheal rings started to degenerate, which could have caused pressure necrosis. Additionally, the presence of complete tracheal rings would prevent any stretch in the trachea, unlike in mammals where the fibroelastic membrane and trachealis muscle can elongate in response to stress, making an exact fit more critical in birds.

Day 401 was the first recorded day nebulization was used with dexamethasone sodium phosphate. Despite the potential risks and adverse effects involved with the use of corticosteroids, the owner felt the patient responded best to a combination of saline, acetylcysteine, and dexamethasone sodium phosphate. Corticosteroids were continuously used after stent placement, at very low doses (0.032 to 0.064 mg/mL q24h to q48h and q12h to q24h during flare-ups). Other recommendations in humans include continued management of stented tracheas with periodic use of balloon dilation or other procedures to continue to maintain a patent airway because of repeated buildup of exudates or obstruction of the lumen by granulation tissue. (21) Data are conflicting on the use of bronchodilators for tracheomalacia; some studies have shown that they are contraindicated because they relax tracheal smooth muscle and may worsen collapse in malacic tracheas. (22) Results of other studies that evaluated the effects of inhaled (32 agonists on lung function in infants with malacia or recurrent wheeze indicated that infants with malacia were no more likely to worsen after inhaled bronchodilator administration than those without malacia. (23) In this case, a nebulized bronchodilator was used initially for several days, before any radiographic or endoscopic evidence of tracheomalacia; however, no clinically obvious benefits were observed.

Stent placement was a success because the owner was able to manage the respiratory clinical signs with adjunctive nebulization for more than 22 months. Before stent placement, medical therapy alone was insufficient. Long-term nebulization medical therapy may be necessary with stent placement to decrease respiratory clinical signs; however, the inclusion of steroids cannot be recommended in birds. Because corticosteroids are contraindicated in birds, they are not an appropriate medical option until all other anti-inflammatory options have been exhausted. In this case, a submaximal dosage of meloxicam (0.3 mg/ kg q24h) was used, and the dose should have been increased before using corticosteroids as a last treatment option. A higher dosage of meloxicam (1 mg/kg q12h) for a longer period is recommended before considering the use of corticosteroids. (24) The quality of life provided to this bird for 22 months indicates that intraluminal tracheal stenting has the potential to be a viable option for avian veterinary patients with tracheal stenosis. In these cases, we recommend continued surveillance for potential stent-associated complications.

Acknowledgments: We thank Ashley Schuller and Carole McElhannon for their technical assistance, Drs Elizabeth Howerth and Monique Franca for evaluating the histopathologic results, and the UGA Veterinary Histology Laboratory for assistance with histologic sectioning. We also thank Dr Steve Mehler who helped design the stent.

Johanna Mejia-Fava, PhD, DVM, Shannon P. Holmes, DVM, MSc, Dipl ACVR, MaryAnn Radlinsky, DVM, MS, Dipl ACVS, Dan Johnson, DVM, Dipl ABVP, Angela E. Ellis, DVM, PhD, Dipl ACVP, Jorg Mayer, Dr Medvet, MSc (WAH), Dipl ABVP, Dipl ECZM, Dipl ACZM, Rodney Schnellbacher, DVM, and Stephen J. Divers, BVetMed, Dipl ZooMed, Dipl ECZM, Dipl ACZM, FRCVS

From the Department of Small Animal Medicine and Surgery (Mejia-Fava, Divers, Schnellbacher, Radlinsky, Mayer), Athens Veterinary Diagnostic Laboratory (Ellis), and Veterinary Biosciences and Diagnostic Imaging (Holmes), College of Veterinary Medicine, University of Georgia, 2209 College Station Road, Athens, GA 30602, USA; and Avian and Exotic Animal Care, 8711 Fidelity Dr, Raleigh, NC 27617 (Johnson). Present address (Schnellbacher): Dickerson Park Zoo, 1401 W Norton Rd, Springfield, MO 65803, USA.


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Author:Mejia-Fava, Johanna; Holmes, Shannon P.; Radlinsky, Mary Ann; Johnson, Dan; Ellis, Angela E.; Mayer,
Publication:Journal of Avian Medicine and Surgery
Article Type:Clinical report
Date:Sep 1, 2015
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