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Brachycephalic dog breeds are becoming increasingly popular pets among the Australian public, with the well-known pug breed a leading choice. This popularity has been attributed to what’s known as ‘kindchenschema’, where owners observe features in their pet that mimic those seen in human infants. This correlation endears the animal to the owner. But these features—large eyes, wider, rounder heads—are also the cause of significant conformation-related respiratory disorders, such as brachycephalic obstructive airway syndrome (BOAS).1
While structural upper respiratory disorders are common in brachycephalic breeds, the prevalence of conditions such as neoplasia tend to be more commonly associated with their dolicocephalic (long muzzle) counterparts. It is hypothesised that this is due to the greater sinonasal area for environmental toxins to cause disease in dolicocephalic breeds.2, 3
Despite the fact that brachycephalic breeds are underrepresented in many types of upper respiratory neoplasias, these conditions must always remain on their differential diagnoses list for dyspnoeic presentation. In assessing dyspnoeic patients, it is important to acknowledge that the presence of discharge, particularly mucoid discharge, may hint towards underlying infectious or neoplastic disease processes, but on their own, remain a non-specific clinical finding. 4, 5
An example of the importance of a broad differential diagnoses list and careful physical examination involved an eight-year-old male neutered pug that presented to the general practice veterinarian at Cheltenham Veterinary Clinic for upper respiratory issues. The patient was reported to have had serous discharge noted from one nostril over the previous two months, with a progression of clinical signs leading to the development of mucoid nasal discharge in the contralateral nostril in the 24 hours preceding their veterinary consultation.

Physical examination found the patient to be panting with mildly injected oral mucous membranes, and bounding femoral pulses. This combination of findings suggested cardiovascular distress resulting from upper respiratory disease. The severity of the signs was clinically suspected to have been exacerbated by the presence of pre-existing BOAS. The remaining physical examination findings were unremarkable, with no obvious facial asymmetry detected.
A sample of the mucoid nasal discharge was prepared on a glass slide using Diff-QuikTM staining before being viewed under compound microscopy. In-house microscopy revealed a dense population of mononuclear cells at x100 oil-immersion resembling either lymphocytes or neoplastic cells, or both.
A combination of clinical history, physical examination findings, and cytological abnormalities increased suspicion of a neoplastic process. In general, sinonasal tumours are considered rare in canine patients.6 Of these nasal neoplasia cases, the majority are carcinomas, with adenocarcinomas being the most prolific.7, 8
There is currently a paucity of literature documenting canine frontal sinus carcinomas (FSCs).9
Given the signs of cardiovascular compromise in the patient, the decision to refer for specialist stabilisation and investigation through advanced imaging and sampling under general anaesthesia was made. As even the most routine of procedures requiring general anaesthesia are considered high risk in brachycephalic breeds, the involvement of an anaesthetist in the patient’s management was considered prudent.10 In more stable patients, it would be appropriate to submit the sample of nasal discharge for review by a specialist pathologist before progressing along a step-wise diagnostic pathway.

The patient presented to Southpaws Specialty, Emergency and Referral Hospital, later that same day and was immediately assessed by the head of the emergency department.
Clinical findings at the time of presentation suggested that the patient was haemodynamically stable, despite audible breed-related stertorous upper respiratory sounds, and the presence of nasal discharge. The patient was discharged home with oral Cerenia (maropitant) tablets, and oral omeprazole.
The following morning, the patient was admitted to hospital for advanced imaging in the form of computed tomography (CT) scanning, and rhinoscopy under general anaesthetic. The patient was pre-medicated with 5mcg/kg medetomidine and 0.1mg/kg methadone intramuscularly (IM). An intravenous (IV) cannula was placed once sedate, and the patient was induced with propofol titrated to effect before being intubated with a 5.5 endotracheal tube and maintained on inhalational anaesthesia (isoflurane and oxygen).
As part of a brachycephalic protocol, the patient received pantoprazole 1mg/kg slow IV, and ondansetron 0.5mg/kg IV in addition to the maropitant administered at home the night before.11, 12, 13, 14
Throughout the anaesthetic, the patient required a single dose of glycopyrrolate at 5mcg/kg IV in response to a hypotensive event, and was noted to be hypothermic throughout, requiring active warming.
The CT scan was performed, with in-house interpretation identifying a soft tissue attenuating mass in the right nasal cavity. Invasion into the caudal aspect of the contralateral nasal cavity and nasopharynx was noted. There was no noted evidence of metastasis at the time of the preliminary scan.
Bilateral rhinoscopy was performed using a 1.9mm rigid 30-degree angle endoscope. This procedure revealed a significant build-up of mucopurulent discharge in the right nasal cavity, accompanied by significant mucosal hyperaemia, oedema, and proliferative tissue that appeared to be occluding the nasal meatuses. The left nasal cavity appeared largely unremarkable.
A blind biopsy technique was utilised to collect samples of the abnormal right nasal mucosa, and fine needle aspirates (FNAs) of the right submandibular lymph node were performed and sent to a specialist pathologist for analysis.
The patient recovered from the general anaesthetic smoothly without complication and was discharged home later the same day.
The patient was sent home with the following medications:
• Meloxicam 0.1mg/kg orally (PO) every 24 hours for five days
• Omeprazole 10mg PO every 12 hours for seven days
• Maropitant 24mg PO every 24 hours for one dose after the dose given the night before
While in hospital, the patient received a single subsequent dose of methadone 0.1mg/kg IV, and paracetamol 10mg/kg IV slow as a single dose for pain management.
Cytopathological analysis of the right submandibular lymph node FNAs demonstrated mild reactive lymphoid hyperplasia and neutrophilic lymphadenitis, with no evidence of metastatic neoplasia observed. The histopathological assessment of the submitted biopsies enabled a diagnosis of nasal adenocarcinoma to be reached (Figure 1). This type of neoplasia is noted to be locally aggressive but rarely metastasises. In cases where it does, the most common predilection sites for this are the lungs and regional lymph nodes.
Following this diagnosis, the patient was referred to the internal oncology department, where the process was further explored, and the following treatment options discussed:
• Radiation thapy1, 5
• Toceranib phosphate (TOC)9
• Chemotherapy with either carboplatin or doxorubicin administration16, 17
The decision was made to proceed with classic chemotherapy, with carboplatin selected as the agent of choice. One week post administration of the carboplatin, the patient was presented for a neutrophil nadir to be performed in order to assess his resulting immunosuppression from the medication.17 The patient was seen every three weeks for repeat carboplatin administration following in-house blood work, with particular focus on his neutrophil count, and any other abnormalities that may have arisen.
Following the patient’s fourth chemotherapy dose, a repeat staging CT scan was performed, with the images sent to a veterinary radiologist for interpretation. The changes noted on the scan indicated slight reduction in mass size, with evidence of disease stabilisation. The chemotherapeutic course was commenced on a monthly basis for a total of five further treatments. Treatment at the initial specialist hospital ceased when the oncology department closed.
Throughout the course of treatment, the patient had mild, stable non-regenerative anaemia, and persistent low grade nasal discharge, but no other significant adverse effects were noted.
Guidelines suggest that the median survival time (MST) is three to six months for surgery, chemotherapy, immunotherapy, cryosurgery, and no treatment. MST increases to eight to 23 months for radiation therapy +/- surgical debulking.18, 19
The patient is currently being managed palliatively on Meloxicam 0.1mg/kg PO q24hrs and medical cannabidiol oil on an as-needs basis, 18 months after initial presentation.9, 20 The owner reports a good quality of life with this medical regime.
References:
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2.. Hayes HM, Jr., Wilson GP, Fraumeni HF, Jr. Carcinoma of the nasal cavity and paranasal sinuses in dogs: descriptive epidemiology. Cornell Vet 1982;72:168-179.
3. Reif JS, Cohen D. The environmental distribution of canine respiratory tract neoplasms. Arch Environ Health 1971;22:136-140.
4. Cohn LA. Canine nasal disease. Vet Clin North Am Small Anim Pract 2014;44:75-89.
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18. Oncology VSoV. NASAL CAVITY TUMORS – CANINE. 2019:https://vsso.org/nasal-cavity-tumors-canine.
19. Henry CJ, Brewer WG, Jr., Tyler JW et al. Survival in dogs with nasal adenocarcinoma: 64 cases (1981-1995). J Vet Intern Med 1998;12:436-439.
20. Henry JG, Shoemaker G, Prieto JM, Hannon MB, Wakshlag JJ. The effect of cannabidiol on canine neoplastic cell proliferation and mitogen-activated protein kinase activation during autophagy and apoptosis. Vet Comp Oncol 2021;19:253-265.


