Introduction

Brachycephalic obstructive airway syndrome (BOAS) is a term that encompasses the anatomical abnormalities associated with the conformation of brachycephalic breeds of dog. Anatomical problems include stenotic nares, enlarged tonsils, elongated soft palate, everted lateral saccules of the larynx, narrowed rima glottides, and collapse of the larynx and trachea.¹

Surgical management by rhinoplasty, palatoplasty, laryngeal sacculectomy, and/or arytenoid laryngoplasty may be effective in improving quality of life in affected animals, but anesthetic management can be difficult. A temporary tracheostomy may be required to relieve dyspnea caused by upper airway swelling and obstruction in the recovery period. However, tracheostomy tubes are associated with a high risk of complications, such as obstruction, dislodgement, infection, severe sinus bradycardia, hyperthermia, and potential death.²

Reduction in edema of the larynx may be a less invasive way of managing any upper respiratory tract obstruction. Administering adrenaline via a nebulizer to reduce inflammation may circumvent the need for tracheostomy.

Case Report

A 7 yr old female spayed pug weighing 6.7 kg was presented with a 2 mo history of worsening inspiratory stertor/stridor and an acute episode of severe dyspnea, cyanosis, and collapse 24 hr previously. On presentation she was very bright and lively with a body condition score of 6/9. Respiratory rate and heart rate were within normal limits at 20 beats per min and 110 beats per min, respectively, at rest, but inspiratory stertor was apparent even at rest. She had a lifelong history of infrequent regurgitation and retching, although this had not occurred for several wk prior to admission.

Diagnosis and Management

A combination of 0.2 mg kg⁻¹ methadone^a and 1μg kg⁻¹ dexmedetomidine^b was administered via an intravenous catheter 30 min before induction of anesthesia using 2mg kg⁻¹ propofol^c. Examination under a light plane of anesthesia revealed stenotic nares, an overlong soft palate, everted laryngeal saccules and grade III laryngeal collapse. No erythema or edema of the palate was evident. Thoracic and neck radiographs confirmed a severely thickened soft palate measuring 1.6 cm in width, but were otherwise unremarkable. Endotracheal intubation with a 5.0 mm tube was uneventful, and anesthesia was maintained with isoflurane^d in oxygen delivered in a circle system. Intra-operative monitoring included assessment of the echocardiogram, noninvasive blood pressure, peripheral capillary oxygen saturation (SpO2), temperature, and end-tidal CO₂ and inhalational agent concentrations. The patient was positioned in sternal recumbency for the duration of the anesthetic, and was mechanically ventilated. Rhinoplasty, laryngeal sacculectomy, palatoplasty, and a left-sided laryngeal tie-back were performed without extubation and with no complications. Dexamethasone^e 0.2mg kg⁻¹ and potentiated amoxicillin^f, 20mg kg⁻¹ were administered intravenously.

Sixty min after induction of anesthesia the surgical procedure was complete and the isoflurane was discontinued. Oxygen was continued at 2 L min⁻¹ for 15 min when the dog no longer tolerated the endotracheal tube. Peripheral capillary oxygen saturation (SpO2) at this time was 96% as measured by the pulse oximetry probe on the dog's tongue. However, the dog quickly became distressed and dyspneic after extubation. 2.5mg phenylephrine^g diluted in 5ml saline was nebulized^h and dexmedetomidine 1.5 μg kg⁻¹ was administered intravenously. Flow by oxygen was also started at 4 L min⁻¹. Respiration initially improved, but within 20 min she again became distressed, dyspneic, and cyanotic. Upper airway examination, performed under laryngoscopy following propofol 3 μg kg⁻¹ IV, showed swelling around the larynx and obstruction of the upper airway by the swollen soft palate. Adrenaline 0.3 mg diluted in 5 ml sterile saline was administered via nebulization for 10 min (Figure 1). An IV infusion of dexmedetomidine at 1μg kg⁻¹ hr⁻¹ was started to provide sedation and reduce the risk of excitement worsening the dynamic obstruction. After nebulization with adrenaline inspiratory respiratory effort improved and mucous membrane color returned to normal. Nebulization with adrenaline for 10 min was repeated every 6 hr over the following 24 hr period and the dexmedetomidine infusion was continued for 12 hr. Oxygen supplementation was not required after nebulization with adrenaline was initiated, based on respiratory effort, respiratory rate, mucous membrane color, pulse oximetry, and the dog's demeanour. The dog was discharged with oral prednisoloneⁱ 1 mg once a day. Two mo after the procedure, the dog had made a good recovery but was still becoming dyspneic on exertion. On examination under anesthesia, the right side of the larynx could be seen collapsing across the midline and there was narrowing of the rima glottis. A right-sided laryngeal tie-back was performed using the same anesthetic and nebulization protocol and 6 mo later, the dog has returned to normal quality of life with no further respiratory problems reported.

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Discussion

BOAS and laryngeal collapse at grade II or III in dogs carries a guarded prognosis. Although surgical management can be successful, the most common postoperative complication is dyspnea, thought to result from a combination of pharyngeal edema, collapse of laryngeal structures, and reduced pharyngeal muscle tone associated with anesthesia. Respiratory complications are reported as an underlying cause of anesthetic-related deaths in 30–40% of dogs, with respiratory obstruction the principal cause of respiratory complications in brachycephalic breeds.^3,4 Excitement can increase inspiratory effort and result in dynamic collapse of some of the components of the upper respiratory tract, therefore worsening the aerodynamic flow. Severe dyspnea necessitates the placement of tracheostomy tubes in up to 53% of dogs undergoing surgery for BOAS with associated stage II or III laryngeal collapse.⁵ Complication rates associated with tracheostomy tubes in dogs have been reported as high as 86%.² Clearly such a high complication rate can have significant consequences, and a failure rate of tracheostomy of 19% has been reported, resulting in euthanasia or death of affected dogs.²

In dogs with BOAS but without laryngeal collapse, temporary tracheostomy tubes are also often required to manage the pharyngeal edema and inflammation in the postoperative period. The risks of postoperative airway obstruction (necessitating a tracheostomy tube) are decreased by the use of peri-operative intravenous corticosteroids, which may reduce edema by downregulating the recruitment and action of inflammatory cells as well as decreasing capillary vessel dilation and permeability. Although theoretically helpful, firm evidence to show reduction in laryngeal edema after intubation or surgery is lacking. Sedation, usually with α₂-agonists such as dexmedetomidine, may be used postoperatively to minimize stress on recovery and prevent vocalization or increased respiratory rate and effort contributing to dynamic airway obstruction and worsening edema. In this case, the prolonged sedation may have been beneficial whilst edema resolved; however, initially it was not sufficient to prevent dyspnea and cyanosis. Sedation is often not recommended for brachycephalic patients due to relaxation of laryngeal musculature and the risk of regurgitation, but often the decreased respiratory rate is beneficial overall to aerodynamic flow. The potent vasoconstrictive effects dexmedetomidine may have also played a role in the reduction of laryngeal edema. However, to the author's knowledge this has not been previously demonstrated in dogs, and the initial phenylephrine nebulization and administration of dexmedetomidine was not sufficient to control the dypsnea in this case.

Nebulization of racemic adrenaline has been recommended for upper airway obstruction due to laryngotracheobronchitis and postintubation laryngeal edema in children, and has also been reported to be effective in adults with upper airway obstruction.^6,7 Adrenaline binds to the α-adrenergic receptors on vascular smooth muscle cells, activating these receptors and resulting in localized vasoconstriction and decreased blood flow. This minimizes the formation of edema, therefore reducing the risk of airway obstruction after extubation. When there is marked laryngeal obstruction, it is possible that nebulization will only affect the immediate area it comes into contact with, but, as the edema reduces, the nebulized drug will be carried further down the tracheobronchial tract.

Unlike phenylephrine, which acts on α₁-adrenergic receptors, nebulization of adrenaline may also stimulate β-adrenergic receptors, leading to bronchiole relaxation. Under general anesthesia, atelectasis can occur in the dependent lung, but an increase in airway resistance due to partial upper airway obstruction may lead to hypoventilation and prevent alveolar expansion. Negative pressures created within the thorax by inspiration against a partially obstructed larynx may also lead to transient pulmonary edema, further worsening any hypoxemia. Bronchiolar dilation may help to improve ventilation and minimize the increased respiratory effort that can worsen postsurgical laryngeal edema.

The risks of adrenaline nebulization are not fully known, although rebound edema is recognized in human patients, and systemic side effects may be seen in patients with heart disease if sufficient concentrations of adrenaline enter the systemic circulation.⁸ Rebound edema may result from prolonged use of adrenergic agonists that act on both α and β receptors, such as adrenaline. Initially, the α₁ adrenergic effects will dominate, causing vasoconstriction, but this effect may fade over time. Subsequently, the effects of stimulation of β receptors results in vasodilation and increased edema and secretions. No adverse reactions were seen in this case, although only a short duration of treatment was required.

The risk of rebound edema may be minimized by using selective α-adrenergic agonists such as phenylephrine. Intranasal edema following anesthesia in horses can be treated using intranasal phenylephrine.⁹ However, in this case there was no improvement in upper respiratory tract obstruction following nebulized phenylephrine, whereas a marked improvement was seen following the next nebulization when adrenaline was used, which may be due to the contribution of stimulation of β₂ receptors resulting in smooth muscle relaxation and subsequent bronchodilation.

Nebulized adrenaline in children has been shown to have minimal systemic effects if doses lower than 3 mL of adrenaline (1:1000) are used. No significant increase in heart rate and no statistically significant increase in systemic arterial blood pressure were seen in children with acute inflammatory obstruction of the airways. Of 184 children assessed in one review, no adverse effects were observed.¹⁰ This may be due to the potent vasoconstrictive effects of adrenaline on the respiratory mucosa limiting systemic absorption and, therefore, also limiting the β₁-adrenergic effects such as tachycardia.¹⁰

Conclusion

Nebulization with adrenaline has not previously been reported in dogs. It may be appropriate in cases of postoperative upper airway obstruction following surgery for BOAS, and may prevent the need for a tracheostomy, but further investigation is warranted.