Brachycephalic airway syndrome

Adjunct Professor Philip A Moses BVSc, Cert SAO, FANZCVS Specialist Small Animal Surgeon Founder Veterinary Specialist Services Underwood, Jindalee, Toowoomba and Gold Coast, Queensland Australia www.vss.net.au

The popularity of brachycephalic dogs has increased tremendously over the past 10 years – in particular French Bulldogs – now the most popular breed in the UK and among the most popular breeds worldwide. This widespread popularity has highlighted the many problems of these little dogs. From an evolutionary point of view all dogs have descended from the wolf – although looking at a Pug, Frenchie or Bulldog this is difficult to believe.

This series of three short presentations looks at the pre-operative assessment, relevant surgical procedures and post-operative management of brachycephalic airway syndrome.

PATHOPHYSIOLOGY

There is no definitive list of the brachycephalic breeds however I think most are included below:

Affenpinscher American Bulldog Australian Bulldog Boston Terrier Boxer Brussels Griffon Bulldog Bullmastiff Cavalier King Charles Spaniel Cane Corso Chow Chow Dogo Argentino Dogue de Bordeaux English Toy Spaniel French Bulldog Japanese Chin Lhasa Apso Neapolitan Mastiff Pekingese Presa Canario Pug Rottweiler Shar-Pei Shih Tzu Tibetan Spaniel Valley Bulldog

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Brachycephalic airway syndrome is also reported in cats with a brachycephalic conformation - Persian and Himalayan.

In brachycephalic animals the skull is shortened rostrally with dorsoventral compression of the nasal passages as well as loss of or dramatic compression of the frontal and maxillary sinuses. There is distortion of pharyngeal and laryngeal soft tissues increasing airway resistance in the upper airway. Selective breeding has worsened this condition significantly over time.

The brachycephalic skull – changes over time

1870 2010

Primary components of BAS: - stenotic nares - elongated soft palate - oedematous laryngeal ventricles / laryngeal collapse - choanal hypoplasia - macroglossia - tracheal hypoplasia - obstructive nasal turbinates – recently described

Stenotic nares, choanal hypoplasia, elongated soft palate, tracheal hypoplasia and obstructive nasal turbinates are considered primary anatomical components of BAS. Excessive negative pressure during inspiration, through the obstructed nares and pharynx, causes inflammation and mucosal oedema, and results in further stretching of redundant tissue and eventual eversion of laryngeal ventricles and collapse of the larynx.

Note – Tracheal hypoplasia is not associated with BAS but will contribute to airway distress in brachycephalic breeds. Tracheal hypoplasia is determined by the ratio of the trachea to the thoracic inlet. The normal ratio is 0.2, less than 0.16 is regarded as tracheal hypoplasia. The breed average in the British Bulldog is 0.106.

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Brachycephalic airway syndrome is also associated with reflux oesophagitis and hiatal hernia secondary to increased intra-thoracic pressure.

Secondary components of BAS: Oedematous laryngeal ventricles Laryngeal collapse Pharyngeal hyperplasia Tracheal collapse Bronchiectasis and bronchial collapse Choanal collapse Hiatal Hernia Gastro-oesophageal reflux

Early surgical intervention is essential to help reduce secondary changes.

CLINICAL SIGNS

Clinical signs are highlighted by inspiratory dyspnoea, usually worsened by exercise and high ambient temperature. Dyspnoea is primarily inspiratory if only the external nares and turbinates are involved, however there is an inspiratory and expiratory pattern with involvement of the choanae, pharynx, soft palate and eventually the larynx.

Cyanosis, hyperthermia and collapse may result from increased activity as animals work harder to breathe. These animals often present for noisy breathing, snoring, dyspnoea or hyperthermia.

Inspiratory dyspnoea, often with open-mouth breathing. The wings of the nostrils fill the external nares and are sucked inward on inspiration, occluding the nostril. Other signs may include gagging, coughing, difficulty in eating and inspiratory stridor associated with obstructed nasal passages and an elongated soft palate. Approximately 45% of dogs will develop gastrointestinal signs in the first year of life associated with increased abdominal pressure. Reflux oesophagitis and hiatal hernia are commonly seen. Clinical signs worsen with age and exercise. Most brachycephalic dogs require assessment and corrective / reconstructive surgery; ideally this should be undertaken at 12 months of age and before 2 years of age – this helps to prevent the development of secondary changes.

Warning – it is our preference to undertake definitive corrective procedures at the same time as assessment and examination under anaesthesia. Otherwise anaesthetic recovery in a dog with compromised airways may be problematic.

PRE-OPERATIVE ASSESSMENT

It is not possible to assess the airways – other than the nares, in a conscious dog. A complete assessment of brachycephalic dogs prior to surgery is essential for attaining the best possible outcome and to give the animal’s owners the most accurate prognosis.

Prior to surgery we recommend the following assessment be undertaken: Pedigree – record of the dog’s pedigree is essential for information gathering purposes. History – a thorough clinical history including diet, previous and current illness and medications. Physical examination – include auscultation of the sinuses, larynx, pharynx as well as the thorax.

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Neurological examination – essential due to the high incidence of hemivertebrae and encephalopathies. Haematology / biochemistry / blood gasses – biochemical and haematological analysis prior to anaesthesia is essential prior to any anaesthetic induction. Ophthalmological examination – brachycephalic dogs have many eye issues Musculoskeletal examination – many orthopaedic conditions are commonly seen in brachycephalic dogs – in particular medial patella luxation and hip dysplasia. Imaging minimum database is thoracic radiology however assessment by whole body CT is our preferred imaging modality

Once all data is available a veterinarian can develop an assessment of the risk of brachycephalic surgery and have a discussion with the owner of the dog about these risks so that informed consent may be obtained.

DIAGNOSIS Clinical signs of obstructive breathing are common, auscultation especially over the larynx as thoracic auscultation is complicated by referred upper airway sounds. In the UK some centers advocate Exercise Tolerance Testing however in the heat and humidity of Brisbane running a Pug up and down the carpark would not end well. For me the most telling diagnostic test is the presence of Grade 1 laryngeal collapse – if a dog has oedematous laryngeal ventricles – it has significantly increased inspiratory pressures – enough to lead to laryngeal collapse. This is my diagnostic test for the requirement for surgery.

RADIOLOGY Cervical area: elongated soft palate extending into the rima glottides. It is essential to evaluate the tracheal diameter as a hypoplastic trachea significantly worsens prognosis. The normal tracheal diameter-to-thoracic inlet ratio is 0.2 The tracheal diameter-to-thoracic inlet ratio in normal British Bulldogs is 0.106 Presence of hemivertebrae – these are common in many of the brachycephalic breeds. The incidence in French Bulldogs is around 80%. Any dog with ANY hemivertebrae (including caudal vertebrae) must NOT be used for breeding.

Tracheal hypoplasia is the ratio of the width of the trachea at the thoracic inlet to the thoracic inlet = X/Y above

YY

X

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British Bulldogs have the highest incidence of hypoplastic trachea (55%) of all the brachycephalic breeds.

Thorax radiography: Hiatal hernia, aspiration pneumonia and pulmonary oedema are very common. If there is evidence of right-sided heart failure an echocardiogram is recommended, particularly if there are radiographic signs of cardiac enlargement, to help assess myocardial function and arrhythmias.

ENDOSCOPY Given the high incidence of oesophagitis, hiatal hernia and other upper GI disorders consideration should be given to routine upper GI assessment in all brachycephalic dogs.

BRONCHOSCOPY Assessment of the trachea to the level of the tracheal bifurcation is important to rule out tracheal collapse. The trachea should be observed along its entirety during both inspiration and expiration. We use a 4mm flexible endoscope and find this instrument adequate for all animals. The same instrument can be retroflexed to examine the choanae.

CHOANAL EXAMINAITON Using a small flexible endoscope retroflexed it is important to examine the choanal region. Abnormalities seen include foreign bodies, aberrant turbinates, infection – fungal and bacterial and the presence of hyperplastic lymphoid tissue.

OROPHARYNGEAL EXAMINATION Examination of the caudal pharynx and larynx requires light general anaesthesia. Neither the depth of anaesthesia nor the anaesthetic agent should depress normal abduction and adduction of the arytenoid cartilages and vocal cords. Acepromazine and barbiturates are best avoided; we use medetomidine and methadone premed and an Alfaxan induction to anaesthetise these animals for oropharyngeal assessment.

The first thing to assess is laryngeal function. We are looking at two things simultaneously. 1 Laryngeal function – regular and symmetrical opening and closing of the larynx. 2 Evidence of laryngeal collapse Grade 1-3. Grade 1 laryngeal collapse is noted as oedematous laryngeal ventricles – white / pink, shiny dome-shaped structures sitting at the base of the vocal cords and occluding the larynx ventrally. Note the ventricle is not OEDEMATOUS, we are seeing oedema of the mucosa of the ventricle.

The soft palate should be examined without an endotracheal tube in place and with the tongue in a normal position as the position of the soft palate can be affected by the position of the head, traction on the tongue and presence of an endotracheal tube. The soft palate should not extend beyond the cranial tip of the epiglottis and lateral landmarks are the caudal extent of the tonsillar crypts.

Tonsils should be assessed for hyperplasia and any evidence of redundant mucosal folds in the oropharynx.

Other anomalies include cleft palate – both hard and soft should be assessed, dental abnormalities – retained deciduous teeth and un-erupted teeth as well as oronasal fistulae etc.

COMPUTED TOMOGRAPHY

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ANAESTHETIC CONSIDERATIONS: As previously advised, it is our preference to undertake definitive corrective procedures at the same time as assessment and examination under anaesthesia. Otherwise, anaesthetic recovery in a dog with compromised airways may be problematic.

Screening blood testing – biochemistry and haematology are strongly recommended.

Our routine premedication for brachycephalic dogs is Methadone and Medetomidine

An IV catheter is always placed.

In healthy animals we use a pre-med of - Methadone – 0.2-0.3 mg/kg and Medetomidine 3-5 µg/kg.

Patients are pre-oxygenated for 10 minutes prior to induction of anaesthesia – we find this simple step significantly improves outcomes.

Induction at Veterinary Specialist Services is by Alfaxalone – 1-2mg/kg – to effect.

Following assessment of the upper airways and choanae animals are intubated with a cuffed endotracheal tube and anaesthesia is maintained with Isoflurane 1-2% and Oxygen.

Surgical Procedures:

The most common surgical procedures undertaken (in order of procedure) are:

Resection of the soft palate Resection of oedematous laryngeal ventricles Removal of tonsils Nasal alarplasty

Positioning Animals are positioned in sternal recumbency with the mouth open. We use a tape to hold the head up. See image.

This position seen to the right allows the surgeon to have the best exposure, a head light is preferred over a ceiling mounted light.

Below we can see bupivacaine (1-2mg/kg) being administered as a splash block on the oral mucosa. This provides excellent analgesia for 3-5 hours.

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ELONGATED SOFT PALATE

The normal soft palate extends caudally to the base of the tonsillar crypt and just reaches the epiglottal apex and is only 3-5mm thick. In brachycephalic airway syndrome animals, the soft palate extends beyond the epiglottis into the larynx, blocking air into the larynx and trachea. In severe cases the soft palate may extend into the trachea. Ninety-five percent of elongated soft palate cases are in brachycephalic breeds. The increased respiratory effort to overcome this obstruction causes the soft palate to flutter and vibrate, resulting in stridor. Fluctuations in airway pressure during panting cause turbulence which traumatises the soft palate and results in inflammation, oedema, swelling and further soft palate lengthening and obstruction. This is often accompanied by pharyngeal mucosal oedema and enlarged tonsils.

Photograph showing elongated soft palate in a brachycephalic dog. The soft palate can be long enough to obliterate the lumen of the larynx in severe cases.

Surgical Management

The aim is to shorten the soft palate so the free border is just rostral to the tip of the epiglottis or just covers it when the tongue is in a normal position. The resection is usually just cranial to the base of the tonsillar crypt. It is important not to resect the soft palate excessively as this can result in loss of the normal architecture and make nasal aspiration more likely. Excessive resection of the soft palate may require reconstruction.

An oral approach is used. With the dog in sternal recumbency the mouth is held open with a gag or the head is suspended by a tape from the upper jaw. The tongue is gently extended to expose the oropharynx. Due to the small size of the oral cavity there is a limit to the amount of instrumentation that can be used in the mouth; if the animal is of sufficient size malleable retractors may be used to reflect other soft tissue structures.

Careful assessment is required to determine the amount of tissue required to be resected.

There are many ways to undertake this procedure. My usual approach is to resect then suture. Having used all the different techniques over the past 20 years I find that cutting and suturing has the best outcome – both short and long term, and the lowest frequency of complications.

Prior to surgery a dose of bupivacaine is dribbled into the area – bupivacaine is readily absorbed across the mucous membranes.

The free border of the soft palate is grasped with rat toothed forceps, using long scissors the soft palate is carefully cut to the desired length. This is accomplished from the animal’s left toward the right and done quickly. Depending on the level of anaesthesia the remaining palate may spasm and appear shortened.

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The soft palate is then sutured using fine, soft monofilament absorbable suture material. My preference is 5/0-6/0 Monosyn Quick from BBraun with a 16mm 3/8 reverse cutting needle. Suturing facilitates normal healing, also helps with haemostasis and may reduce the incidence of stricture. The oral mucosa should be sutured to nasopharyngeal mucosa and the muscularis layer avoided. The sutures are placed through the oral and nasal mucosa in a continuous pattern but not through muscularis, 1mm from cut edge and 2mm apart.

There are small branches of the tonsillar artery laterally and these should be avoided if possible; haemorrhage can be profuse. Haemostasis is essential - do not complete the procedure unless haemostasis has been achieved. Do not use electro cautery in this area – if there is haemorrhage that is not controlled by pressure or clamping then ligation of the vessel should be undertaken. In my experience excessive use of electro cautery can lead to significant swelling.

Other techniques:

Folding Flap Palatoplasty If the soft palate is excessively thickened – as assessed by CT prior to surgery – then a folding flap palatoplasty may be considered. This technique was described by J. Dupris and is technically quite a challenging procedure – published in 2013 in Clinician’s Brief: https://www.cliniciansbrief.com/article/brachycephalic-syndrome-innovative-surgical- techniques

Ligasure A Ligasure is a bipolar vessel sealing device and may be used, in some cases, for soft palate resection. Great care must be taken as the device may have increased post-operative swelling and scarring complications.

Surgical Laser A carbon dioxide laser may be used for resection of elongated soft palate in brachycephalic dogs. Laser surgery is significantly quicker and has the advantage of good haemostasis, good analgesia and accurate cutting. Again, care must be taken as the device may have increased post-operative swelling and scarring complications.

OEDEMATOUS LARYNGEAL VENTRICLES This is a secondary condition and occurs in brachycephalic breeds with a history of prolonged or repeated airway obstruction. The mucosal lining of the laryngeal ventricles becomes oedematous due to prolonged excessive negative pressure at the ventricular orifice during increased inspiratory effort. This is a direct result of the stenotic nares and elongated soft palate. Mucosal prolapse results in oedema and obstruction of the ventral rima glottis. The oedematous laryngeal ventricles appear as small pink or white masses rostral to and often obscuring the vocal cords.

Severe eversion of the laryngeal ventricles – grade I laryngeal collapse. This dog has already had soft palate resection to allow visualisation of the oedematous laryngeal ventricles.

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Surgical Management Eversion of the laryngeal ventricles is treated by per oral amputation with long-handled instruments. Electro cautery is avoided as this will increase inflammation and may lead to damage to the larynx. Haemorrhage is usually minimal and may be prevented by twisting the ventricle before amputation and controlled with pressure with either swabs or cuffed endotracheal tube.

Technique: The ET tube is removed and anaesthesia maintained by IV dosage if required. The oedematous ventricle is grasped at its apex with a long-handled pair of rat toothed forceps. The ventricle is then resected starting ventrally and proceeding dorsally. Great care is taken to avoid damage to the vocal folds. This procedure is then repeated on the other side. It is essential that the mucosal surface ventrally is NOT DAMAGED. This will lead to cicatrix formation and closure and occlusion of the larynx over time. The resultant laryngeal webbing is very difficult to treat.

Complications Haemorrhage, aspiration pneumonia and pharyngeal oedema.

Excessive intraoperative haemorrhage is rare and can cause aspiration pneumonia. Pharyngeal and laryngeal oedema can be life-threatening. It can be difficult to differentiate between vocal cords with chronic inflammation and inflamed laryngeal ventricles. If in doubt leave them and do no damage. Inadequate tissue removal may be encountered, it is important to have a good field of vision and lighting. A head light is recommended as ceiling mounted lights tend to cast shadows.

LARYNGEAL COLLAPSE – PROGRESSION TO END STAGE DISEASE.

Laryngeal paralysis is caused by the loss of supporting function of the laryngeal cartilages. This condition represents an advanced and critical state of BAS and chronic airway obstruction.

Stage 1 Laryngeal ventricle oedema (see above) into glottic cavity. There is abnormal negative pressure at the glottis during inspiration resulting from increased inspiratory effort necessary for the dog to ventilate through its stenotic nares and elongated soft palate. The resultant mucosal oedema and inflammation lead to laryngeal ventricle eversion and significantly worsen dyspnoea.

Stage 2: The cuneiform process of the arytenoid cartilage weakens and collapses into the laryngeal lumen.

Stage 3: The corniculate process of the arytenoid cartilage collapses towards the midline resulting in complete collapse of the larynx. The cuneiform and corniculate cartilages are progressively distorted and collapse into the glottal opening by increased negative airway pressure caused by increased inspiratory effort. The aryepiglottic fold can also be weakened and drawn into the glottis. Turbulence and vibrations result in inflammation and oedema of the laryngeal mucosa. The net result is a gradual collapse of the laryngeal opening. Most affected dogs have concurrent tracheal collapse. The condition is irreversible. Laryngospasm or difficulty intubating may occur during examination and an emergency tracheostomy may be required.

Endoscopic view of end stage laryngeal collapse. Note medial deviation of the laryngeal cartilages.

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STENOTIC NARES

Stenotic nares are present in 48% of brachycephalic airway syndrome cases in brachycephalic breeds less than 2 years old and are also reported in brachycephalic cats (i.e. Persian). The external nares are formed by a cartilaginous skeleton covered by thickened epithelium externally and mucosa internally. In BAS animals, the cartilages are shortened, thickened, and medially displaced obliterating the nostrils.

Stenotic nares. These dogs have considerable trouble increasing their inspired respiratory ability. Early correction is essential.

Surgical Management

The wing of the nostril should be examined to determine the extent of resection. The tissue is highly vascular and bleeds profusely. Electro cautery is not recommended as this destroys excessive tissue, delays healing and may increase post-operative pain. Adrenaline soaked cotton-wool buds may assist in reducing haemorrhage, but I usually find quick suturing halts bleeding. A surgical laser is excellent for this procedure, however great care must be taken to avoid iatrogenic damage to the pharynx or larynx.

There are a variety of different surgical corrective techniques.

Vertical Wedge This is the technique I most commonly perform. A vertical wedge (inverted V) is cut in the wing of the nostril and extending caudally to include the alar cartilage. A wedge is resected with a No. 11 Bard-Parker blade in ventromedial and lateral directions with a dorsal apex. The wedge is removed and sutured with 5-0 or 6-0 absorbable suture material on a cutting needle (Monosyn is preferred).

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Vertical Wedge Resection Correction of stenotic nares, in this case I have marked the wedge to be resected with felt tip pen for demonstration purposes. The wedges are then resected with a number 11 scalpel blade. The cut edges are sutured starting with the deep suture first. Suture used is 5/0 Monosyn Quick BBraun 3-4 sutures are placed.

Horizontal Wedge

A horizontal wedge is removed from the medial wing of the nostril towards the lateral surface and then deepened dorso-caudally into the alar fold. A second incision is made horizontally along the rostral surface of the wing of the nostril to divide it into dorsal and ventral segments (two- thirds and one-third, respectively) and then deepened to meet the first incision at the alar fold. The flap of the ventral wing of the nostril remains and is sutured dorsally as above. A noted complication: the second incision can easily cut off the mucosal flap.

Lateral Wedge Resection

Involves resection of the caudolateral border of the wing of the nostril and an adjacent triangle of skin. The apex is caudolateral, the base perpendicular to the ventral edge of the wing, with all points of the triangle converging caudomedially toward the alar cartilage. The free point of the wing is pulled laterally as a rotation flap and sutured to the skin.

Alar Cartilage Resection

A recently described technique where the alar cartilage is cut off at the level of the nasal orifice. Owners seem to cope with the hideous cosmetic result and the resultant nasal opening is excellent. This is not a technique I advocate.

Complications of the above procedures

Haemorrhage can be excessive but usually stops once closure is completed. Dehiscence is usually due to self-trauma. The result is primarily cosmetic however I prefer to repeat the repair rather than allowing healing by secondary intention.

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POSTOPERATIVE MANAGEMENT

The animal must be closely monitored for the next 24-48 hours. At Veterinary Specialist Services / Animal Emergency Services we have a dedicated nurse cage side AT ALL TIMES. In my opinion it is negligent to leave an animal unattended in the 24 hours following BAS surgery.

Our dedicated nursing team stays with our patients for 24 hours post op. BAS patients are NEVER left unattended during the post op-period. Note nasal O2 prongs in place.

Once surgery is completed and other BAS associated problems have been treated 1-2 folded swabs are soaked in 20mld Mannitol per swap and a dose of bupivacaine which is attached to a string or tie and placed in the oropharynx. The animal is then left for 5 minutes with the mouth closed. After 5 minutes the mouth is opened and the swab withdrawn to check for haemostasis.

If there is NO haemorrhage then the swab attached to string or tie is replaced and the animal is transferred to recovery. I prefer to leave the ET tube in place – attached to an O2 line, for as long as possible. A staff member must sit with the animal and closely observe the dog. Once the animal is awake the haemostat and swabs are withdrawn and the animal extubated. Nasal oxygen is maintained for the next hour or until it can be stopped with the animal’s O2 saturation staying above 96%.

The animal MUST be observed for the next 24-48 hours. These animals can rapidly deteriorate and die if unattended. It is not acceptable to undertake this surgery if there is no provision for 24 hour monitoring.

Extubation Our preference is to leave the dog intubated for as long as possible. We like the dog to be awake and even standing before extubation. Interestingly many brachycephalic dogs are happy to sit intubated and conscious for a considerable time. Perhaps they are thinking this is as good as it will get for them!

Nasal Oxygen We recover all dogs on nasal oxygen. An Argyle feeding tube may be used, more recently however we have been using paediatric nasal prongs with great success. A small dose of bupivacaine is placed into each nostril and the nasal prongs are placed prior to recovery. Humidified oxygen is supplied until after extubation! Oxygen is continued and slowly reduced when the dog can maintain oxygen saturation of over 98% on room air.

Medication Antibiotics – only used on the basis of culture and sensitivity Analgesia

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Methadone (duration of activity 4-6 hours) is used as part of the pre-med then as required based on pain scoring

Dyspnoea / increased effort

As dogs recover – if they start to develop mild dyspnoea and increased effort we use some or all of the following medications:

Medetomidine – this drug has been game changer for us at VSS. We have been using micro doses of medetomidine for the past 5 years. We dilute the 1mg/ml from the bottle with saline to make it 100µg/ml – 1 in 10 dilution.

Dose we use of medetomidine 0.5µg / kg give IV as required – this may be increased to 1µg / kg. We also use medetomidine CRI at 1µg / kg / hr

Adrenaline - Adrenaline is administered by nebuliser – 0.4 mg with 5mls NaCl for a 10kg animal

Nebulise with saline every 4-6 hours

Trazadone Particularly in very anxious dogs starting at 2.5-5mg/kg every 6-8 hours – not used with Tramadol

Maropitant If nauseous – 1mg/kg once daily.

Omeprazole 1mg/kg every 12 hours PO – for 4-6 weeks post op depending on severity of GIT signs

Pain relief. We rely on the oral Bupivacaine lasts 6-8 hours. Once the animal is discharged oral opioids (Tramadol) are dispensed for 5-7 days – unless Trazadone is required in which case we use a Fentanyl patch. I avoid NSAID’s in these animals until they are eating. Soft food is usually offered 12 hours after recovery. Owners are advised to avoid any hard food for 2-3 weeks.

Patien t recovering with paediatric nasal O2 prongs – these are very well tolerated by our patients

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COMPLICATIONS Uncontrolled haemorrhage, pharyngeal oedema and aspiration pneumonia are common.

If haemorrhage continues the animal must be re-anaesthetised and vessels ligated to control bleeding. NEVER use electro cautery. Bleeding from a branch of the tonsillar artery is most common. Always ensure there is no haemorrhage at the end of the procedure.

Pharyngeal oedema can lead to severe difficulties in breathing following extubation. If the animal cannot maintain oxygen saturation above 90% on room air or 95% on oxygen then my first approach is to re-anaesthetise and re intubate immediately. The animal is anaesthetised with IV anaesthetic on a CRI. Once a new ET tube is placed the pharynx can be packed with swabs soaked in Mannitol. This may have an osmotic effect and help reduce pharyngeal swelling. After 2-3 hours the CRI is reduced and the animal slowly awakened. If the animal can now maintain oxygen saturation above 90% on room air or 95% on oxygen then the animal is closely monitored for the next 24 hours. If the animal cannot maintain oxygen saturation above 90% on room air or 95% on oxygen then the animal is re intubated and the above procedure repeated. If the tube cannot be removed after a further 2 hours then a temporary tracheostomy is required. A tracheostomy may be required post operatively for animals who cannot be extubated. In our hospital the incidence of this complication is less than 2% - however we warn every owner of this possibility. Animals at greatest risk seem to be older English Bulldogs. The tracheostomy is maintained until swelling has resolved sufficiently to allow resumption of respiration – this can be 2-4 days. Tracheostomy requires a high level of care and maintenance and 24-hour monitoring is essential.

If excessive tissue is removed nasal aspiration of food can occur. This can result in chronic nasal infection and aspiration pneumonia. Excessive tissue removal will require soft palate reconstruction.

PROGNOSIS The prognosis for brachycephalic airway syndrome animals is good if these animals are treated prior to 2 year of age, provided they have only stenotic nares and elongated soft palate and minimal secondary changes.

The prognosis is guarded after 2 years due to secondary changes causing additional airway obstruction and progression of disease to grade 2 laryngeal collapse, tracheal collapse and gastrointestinal signs.

The most severe change is associated with bilateral nasal obstruction and high nasal resistance. This induces degenerative change in the nasal mucous membranes, resulting in an increase in respiratory muscle and bronchial smooth muscle tone and causes increased end-expiratory intrapleural negative pressure, functional residual capacity and pulmonary resistance.

Stenotic nares also affect pulmonary mechanics and induce degenerative changes in nasal mucosa. Severe upper airway disease can cause pulmonary oedema due to reduction in intrathoracic pressure and inadequate pulmonary ventilation can cause reduced arterial oxygen content. Hypoxia is a potent pulmonary vasoconstrictor which results in diversion of blood away from poorly ventilated areas and results in pulmonary hypertension. Pulmonary vasoconstriction and hypertension will result in cor pulmonale and right-sided heart failure

It is essential to understand this as the secondary changes are caused by the two primary abnormalities and worsen with time. If the primary abnormalities can be corrected early then secondary changes do not develop.

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The prognosis appears worse for British Bulldogs due to tracheal hypoplasia.

Some earlier studies reported 10 to 20% intraoperative or immediately postoperative mortality in severely affected cases.

In our experience most dogs will have a relatively happy and functional life following early correction of upper airways. Recurrence of stenotic nares, elongated soft palate, laryngeal ventricle eversion and obstructive nasal turbinates can occur due to ongoing turbulence resulting from naso-pharyngeal anomalies and owners must be advised of such. Aspiration pneumonia is a disastrous complication and must be treated very aggressively – many dogs – especially British Bulldogs do not survive this. Concurrent tracheal collapse significantly worsens prognosis.

A recent paper from VSS Brachycephalic airway syndrome: management of post‐operative respiratory complications in 248 dogs B Lindsay D Cook J‐M Wetzel S Siess P Moses AVJ 09 February 2020

Abstract Objective As ownership of brachycephalic dog breeds rises, the surgical correction of components of brachycephalic airway syndrome (BAS) is increasingly recommended by veterinarians. This study's objective was to describe the incidence of, and strategies for the management of post‐ operative respiratory complications in brachycephalic dogs undergoing surgical correction of one or more components of BAS. Methods Medical records of 248 brachycephalic dogs treated surgically for BAS were retrospectively reviewed for demographic information, procedures performed, post‐operative complications and treatment implemented, hospitalisation time, and necessity for further surgery. Results Pugs, Cavalier King Charles Spaniels and British Bulldogs were the most commonly encountered breeds. Dogs which experienced a complication were significantly older (mean was 5.5 years, compared with 4.1 years [P < 0.01]). Fifty‐eight dogs (23.4%) had complications which included: dyspnoea managed with supplemental oxygen alone (7.3%, n = 18), dyspnoea requiring anaesthesia and re‐intubation (8.9%, n = 22), dyspnoea necessitating treatment with a temporary tracheostomy (8.9%, n = 22), aspiration pneumonia (4%, n = 10), and respiratory or cardiac arrest (2.4%, n = 6). Five of the 22 dogs requiring anaesthesia and re‐intubation deteriorated 12 or more hours after post‐surgical anaesthetic recovery. The overall mortality rate in this study was 2.4% (n = 6). Age, concurrent airway pathology, and emergency presentation significantly predicted post‐operative complications. Conclusion Our data show the importance of close monitoring for a minimum of 24 h following surgery by an experienced veterinarian or veterinary technician. Surgical intervention for BAS symptomatic dogs should be considered at an earlier age as an elective procedure, to reduce the risk of post‐ operative complications.

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REFERENCES AND RECOMMENDED FURTHER READING

Bjorling D, McAnulty J, Swainson S. Surgically treatable upper respiratory disorders. Vet Clin North Am Small Anim Pract 2000:30(6):1227-1251. Brdecka D, Rawlings C, Howerth E, et al. A histopathological comparison of two techniques for soft palate resection in normal dogs. JAAHA 2007;43(1):39-44. Byars SG et al. Association of Long-Term Risk of Respiratory, Allergic, and Infectious Diseases With Removal of Adenoids and Tonsils in Childhood. JAMA Otolaryngology–Head & Neck Surgery, 2018 Canine Brachycephalic Airway Syndrome pathophysiology, diagnosis and non surgical management Trappler M.; Moore K. W. Compendium Continuing Education for Veterinarians 33, 5, 2011 Clark GN, Sinibaldi KR. Use of a carbon dioxide laser for treatment of elongated soft palate in dogs. JAVMA 1994;204(11):1779-1781. Davidson EB, Davis MS, Campbell GA, et al. Evaluation of carbon dioxide laser and conventional incisional techniques for resection of soft palates in brachycephalic dogs. JAVMA 2001;219(6):776-781. Ellison GW. Alapexy: an alternative technique for repair of stenotic nares in dogs. JAAHA 2004;40:484-489. Ginn JA et al. Nasopharyngeal turbinates in brachycephalic dogs and cats. JAAHA 2008; 44(5):243–9. Greenberg MJ, Reems MR, Monnet E. Use of perioperative metoclopramide in dogs undergoing surgical treatment of laryngeal paralysis: 43 cases (1999-2006). Vet Surg2007;36:E11. Harvey CE. Upper airway obstruction surgery. III. Oedematous laryngeal ventricle surgery in brachycephalic dogs. JAAHA 1982;18:545-547. Harvey CE. Upper airway obstruction surgery. VIII. Overview of results. JAAHA 1982;18:567-569. Hedlund CS. Brachycephalic syndrome. In: Bojrab MJ, ed. Current Techniques in Small Animal Surgery. 4th ed. Philadelphia: Williams & Wilkins; 1998:357-362. Hedlund CS. Stenotic nares. In: Fossum TW, ed. Small Animal Surgery. 2nd ed. St Louis: Mosby; 2002:727-730. Hedlund CS. Tracheostomy. Probl Vet Med 1991;3(2):198-209. Hendricks JC. Brachycephalic airway syndrome. Vet Clin North Am Small Anim Pract 1992;22(5):1145-1153. Hobson HP. Brachycephalic syndrome. Semin Vet Med Surg (Small Anim) 1995;10(2):109-114. Holt D. Surgery of the upper airway in the brachycephalic dog. Proc ACVS Symp 1998;1:25-31. Huck JL, Stanley BJ, Hauptman JG. Technique and outcome of nares amputation (Trader’s technique) in immature shih tzus. JAAHA 2008;44(2):82-85. Lindsay B et al & Moses PA Brachycephalic Airway Syndrome: Management of Post-Operative Respiratory Complications in 248 dogs AVJ May 2020 pp173-180 Lorison D, Bright RM, White RAS. Brachycephalic airway obstructions syndrome: a review of 118 cases. Canine Pract 1997;22:18-21. Monnet E. Brachycephalic airway syndrome. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: WB Saunders; 2003:808-813. Oechtering G et al Structural characteristics of the nose in brachycephalic dog breeds analysed by computed tomography. Tieraerztl Prax 2007;35(K):177–87. 7. Pink JJ, Doyle RS, Hughes JM, et al. Laryngeal collapse in seven brachycephalic puppies. J Small Anim Pract 2006;47(3):131-135. Poncet CM, Dupre GP, Freiche VG, Bouvy BM. Long-term results of upper respiratory syndrome surgery and gastrointestinal tract medical treatment in 51 brachycephalic dogs. J Small Anim Pract 2006;47(3):137-142. Poncet CM, Dupre GP, Freiche VG, et al. Prevalence of gastrointestinal tract lesions in 73 brachycephalic dogs with upper respiratory syndrome. J Small Anim Pract 2005;46(6):273-279.

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Riecks TW, Birchard SJ, Stephens JA. Surgical correction of brachycephalic syndrome in dogs: 62 cases (1991-2004). JAVMA 2007;230(9):1324-1328. Schuenemann R, Oechtering G Inside the Brachycephalic Nose: Conchal Regrowth and Mucosal Contact Points After Laser-Assisted Turbinectomy JAAHA; 50:237–246. Torrez CV, Hunt GB. Results of surgical correction of abnormalities associated with brachycephalic airway obstruction syndrome in dogs in Australia. J Small Anim Pract 2006;47(3):150-154. Trader RL. Nose operation. JAVMA 1949;114:210-211. Walter ASJ et al Dolichocephalic versus brachycephalic conchae nasales - a microscopic anatomical analysis in dogs. Proceedings of the XXVII EAVA Congress, 2008.123–24; Budapest, Hungary.

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