Tracheal stenosis following endotracheal intubation in a dog

Abstract

A 2-month-old intact female Rottweiler was presented for investigation of coughing and respiratory distress 9 d after an exploratory laparotomy for intestinal foreign body removal. Tracheal stenosis was suspected by radiography and confirmed with computed tomography (CT) and tracheoscopy. After 1 wk of medical management, clinical signs had resolved and the severity of the tracheal narrowing was markedly improved, as confirmed by radiography and tracheoscopy. Tracheal stenosis is a considerable complication of endotracheal intubation in veterinary medicine and may be medically managed, depending on the severity of the tracheal injury.

Key clinical message:

To our knowledge, this is the first clinical case report of tracheal stenosis resulting from endotracheal intubation in a dog and its resolution after medical management.

Tracheal injury is a known complication of endotracheal intubation. In veterinary medicine, tracheal rupture has been reported as a common complication of post-intubation tracheal injury, more commonly in cats (1–3). Tracheal necrosis without tracheal rupture following overinflation or prolonged endotracheal tube placement was reported in 2 dogs (4,5). Postintubation tracheal stenosis is a common complication of long-term endotracheal tube placement in humans (6), but rarely reported in veterinary medicine. There is only 1 case report in a dog with postintubation tracheal stenosis, which improved with surgical intervention (4). Postintubational mature cicatricial tracheal stenosis requires surgical intervention. It is therefore important to diagnose the stage of disease such as incipient or mature tracheal stenosis (7). Incipient tracheal stenosis results from edema or granulation tissue in the acute or subacute phase, whereas mature tracheal stenosis is due to cicatrization in the chronic phase. In dogs, postintubational incipient tracheal stenosis has not been reported. This case report describes a dog with post-intubation tracheal stenosis and resolution of tracheal stenosis with medical management.

Case description

A 2-month-old intact female Rottweiler was presented to the referral hospital for investigation of a sudden onset of coughing and respiratory distress. The dog had a history of an exploratory laparotomy performed for intestinal foreign body removal 9 d before presentation. No complications were reported during the laparotomy procedure or recovery from anesthesia. There was no current evidence of repeated foreign body ingestion at the time of presentation. On clinical examination, an increase in respiratory effort was noted during inspiration with normal lung sounds auscultated bilaterally. During excitation or agitation, the dog was noted to cough and occasionally exhibited cyanosis. A complete blood (cell) count (CBC) was within normal limits for a young dog.

Thoracic and abdominal radiographs were performed. On the thoracic radiographs, there was a focal dorsoventral narrowing of the caudal cervical to thoracic aspects of the trachea, with the most severe narrowing at the level of the thoracic inlet (Figure 1 A,B). The cardiac silhouette, pulmonary vasculature, and pulmonary parenchyma were within normal limits. In the abdominal radiographs, a few small irregular-shaped mineral opaque and heterogeneous soft tissue opaque materials were present within the stomach, in a few segments of the small intestine, and in the colon. Although diffusely decreased serosal margination due to the age of the patient and possible concomitant small amount of peritoneal effusion hampered the precise evaluation of the gastrointestinal tract, there was no evidence of gastrointestinal obstruction. Therefore, upper airway disease was suspected as the cause of coughing and increased respiratory effort.

Figure 1.

Thoracic radiographs of a dog at initial presentation (A — left lateral view; B — ventrodorsal view) and at 2nd presentation 1 wk after medical management (A — left lateral view; B — ventrodorsal view). Marked focal dorsoventral narrowing of the caudal cervical to cranial thoracic trachea at the thoracic inlet was present at initial presentation (A), but substantially improved at the following study (C). Tracheal diameter was normal in both ventrodorsal views (B, D).

The following day, a cervical and thoracic computed tomography (CT) scan and tracheoscopy were conducted for further evaluation of presumed tracheal disease. The cervical and thoracic helical CT study obtained pre- and triple-phase post-contrast images. The following scan settings were used: helical scan mode; slice thickness, 0.625 mm; helical pitch, 1.0; X-ray tube current, 300 mA; 120 kVp; tube rotation time, 1 s; matrix, 512 × 512; and detail algorithms (Light Speed VCT, GE Medical System). On the CT images, there was a focal irregular circumferential narrowing of the trachea at the level of the C6 and C7 vertebrae, approximately 1.3 cm in craniocaudal length (Figure 2 A,B). A diffuse and multifocal patchy soft tissue attenuation with air bronchograms was present throughout the lungs. Three-dimensional volume rendering using a minimal intensity projection was performed with imaging software (Osirix, Pixmeo SAR). These images highlighted the degree and the morphological characteristics of the tracheal stenosis (Figure 2 C). Tracheoscopy revealed a focal severe (75% collapse of the tracheal lumen) narrowing of the trachea (Figure 3 A). In addition, blood-tinged mucoid material was present in the trachea, and the tracheal wall was edematous and pliable. The mucosal surface was smooth and pink with no evidence of tracheal wall necrosis or observable granulation tissue formation. The trachea was intact and no tracheal tear or rupture was identified. The tracheal stenosis was confirmed by tracheoscopy and suspected to be secondary to previous overinflation of endotracheal tube cuff during the recent surgical procedure. The clinical history, location of the tracheal narrowing, and focal tracheal mucosal injury further supported this conclusion. The pulmonary multilobar alveolar consolidation was considered most likely due to aspiration pneumonia.

Figure 2.

Multiplanar reconstruction (A — dorsal plane; B — sagittal plane) and volume rendering 3-dimensional (C) CT images of tracheal stenosis in a dog. A marked focal irregular but circumferential narrowing of the trachea was present at the thoracic inlet. Motion artifact is more severe in the thoracic cavity.

Figure 3.

Tracheoscopy images of a dog at the initial (A) and follow-up presentations (B). A — An image at the level of the severe tracheal narrowing with 75% collapse of tracheal lumen. The tracheal mucosal surface was edematous with blood-tinged mucoid material. No obvious evidence of tracheal necrosis or granulation tissue was present. B — An image showing the same level of trachea shown in A. Tracheal diameter and edematous appearance were both substantially improved.

Due to the dog’s size and continual growth, medical management was elected and the dog was treated with prednisone [1.1 mg/kg body weight (BW), PO, q24h] for management of the inflammation and edematous swelling evident during tracheoscopy. Tracheoscopic balloon dilation or tracheal stent placement was considered if medical management failed to resolve tracheal stenosis after improvement of inflammation and once the dog was fully grown. In addition, clavamox (18 mg/kg BW, PO, q12h), trazodone (1.8 mg/kg BW, PO, q12h), and fenbendazole (50 mg/kg BW, q24h) were prescribed for the treatment of the aspiration pneumonia, keeping the dog calm, and deworming, respectively.

At the follow-up visit 1 wk later, coughing and respiratory effort were markedly improved. Repeat thoracic radiographs revealed that the diameter of the trachea was markedly larger than before and similar in diameter to the adjacent normal trachea on the radiographs (Figure 1 C,D). A tracheoscopy revealed a substantial decrease in swelling (Figure 3 B) and widening of the tracheal lumen. However, a small amount of persistent mucoid discharge was present within the tracheal lumen. The antibiotic was changed to doxycycline (5 mg/kg BW, PO, q12h) according to the culture and sensitivity. The dose of oral corticosteroid was tapered and continued for 1 wk. In addition, an inhaled steroid (dexamethasone) via nebulization was administered daily for 2 wk in accordance with protocols used in pediatric human patients. No respiratory signs were reported following 2 wk of treatment.

Discussion

Tracheal injury is a common complication of post-intubation. Unlike cats with tracheal rupture (1–3), tracheal necrosis and stenosis (4), or tracheal necrosis (5) without tracheal rupture following tracheal intubation has been reported in dogs. The previously reported tracheal stenosis dog was treated surgically (4). This is the first case report of tracheal stenosis following endotracheal intubation, which was improved with medical management alone.

In the present case, tracheal stenosis was suspected by radiographs, whereas CT allowed extension, location, and severity of the tracheal stenosis to be evaluated. Tracheoscopy confirmed tracheal mucosal injury, an edematous and pliable wall with intraluminal blood-tinged mucoid material. According to the location of the tracheal stenosis and the history of the recent surgery, the previous intubation was suspected as the cause. These findings were similar to experimentally induced tracheal stenosis (8,9). Suspected pathogenesis of tracheal injury and tracheal stenosis following endotracheal intubation was described as follows: capillaries in the tracheal wall are easily collapsed and obstructed by compression from the endotracheal tube cuff. Chondrocytes and chondroblasts are sensitive to oxygen and nutrient deprivation, and ischemic necrosis of mucosa and the cartilage occur after sustained compression of the capillaries; this can lead to destruction of the cartilage framework and fibrogenesis as evidenced by acidophil staining during histopathological analysis (10). Injuries of the tracheal mucosa usually heal if tracheal mucosal and cartilaginous damages are mild. This subacute stage of postintubation tracheal stenosis is considered incipient tracheal stenosis and endoscopically edematous in appearance, which may heal with medical management (7). Contrarily, with severe injury to the tracheal cartilage, tracheal stenosis can result from granulation tissue formation and cicatrization, which requires surgical intervention (7). This is experimentally observed 1 to 2 wk after tracheal injury (11). Outcomes in the experimental study in dogs implied clinical differences between incipient and mature cicatricial stenosis (8). With high cuff pressure, the degree and severity of stenosis suggests mature cicatricial tracheal stenosis, whereas low cuff pressure damage that was able to heal without treatment suggests incipient tracheal stenosis.

In the present case, the degree of tracheal narrowing was severe. However, the tracheoscopically edematous tracheal lumen without evidence of necrosis or granulation tissue formation was indicative of incipient tracheal stenosis, although it had already been 9 d after endotracheal intubation. Therefore, medical management was chosen and tracheal stenosis substantially improved in 1 wk without surgical intervention.

This is the first clinical case report of a dog with presumed incipient tracheal stenosis following endotracheal intubation and resolution with medical management. Tracheal stenosis is a considerable complication of endotracheal intubation in dogs and may be medically managed depending on the severity of the tracheal damage. Multimodality evaluation using radiography, CT, and tracheoscopy were useful to assess severity of postintubation tracheal stenosis. CVJ