Nasal Discharge & Epistaxis in a German Shorthaired Pointer

Elisa M. Mazzaferro, MS, DVM, PhD, Diplomate ACVECC

A 12-year-old, 25.5-kg, spayed female German shorthaired pointer was presented to the emergency service for recurrent unilateral nasal discharge and acute onset of epistaxis.

HISTORY

Lifestyle

The dog was 1 of 3 dogs in the household. She was:

• An indoor/outdoor pet that had not traveled outside the state (Colorado)
• Current on immunizations, but had not received any recently
• Not on routine heartworm prevention.

There was no history of weight loss, change in appetite, excess water consumption, or exposure to vitamin K antagonist rodenticide products. The other 2 dogs were healthy.

Clinical Signs & Diagnostics

The dog had initially been seen at another veterinary hospital 5 months previously. At that time, the primary clinical complaints were a dry hacking cough and serous nasal discharge. Cervical and thoracic radiographs performed at initial presentation revealed no abnormalities.

Previous Treatment

Initial therapy consisted of:

• Prednisone: 10 mg (0.4 mg/kg) PO Q 12 H, tapered over 10 days
• Doxycycline: 150 mg (6 mg/kg) PO Q 12 H for 1 week.

The nasal discharge and cough resolved, but then recurred within 3 to 4 days of discontinuing the medications.

Therapy over the next 5 months included:

• Doxycycline
• Clindamycin
• Acepromazine

Additional Diagnostics & Treatment

Two months after onset of clinical signs, the dog was sedated for nasal cavity flushing. A limited examination of the nares and rostral nasal cavity was performed with an otoscope head; no abnormalities were found. Skull radiographs were also performed and revealed increased radiopacity in the left nasal passage (Figure 1).

Figure 1. Skull radiographs performed 2 months prior to development of epistaxis, showing soft tissue density in the left frontal sinus (arrow).

Antibiotics, glucocorticoids, and sedation did not prevent recurrence or progression of nasal discharge and cough. The unilateral nasal discharge continued, became purulent, and then hemorrhagic. At presentation to the referral hospital, the discharge had progressed to mild to moderate epistaxis.

Other Pertinent History

Three years prior to current clinical signs, the dog had a history of recurrent purulent nasal discharge secondary to inhalation of hay seeds into the nasal cavity. Nasal discharge and sneezing resolved after the nasal cavity was flushed with saline.

PHYSICAL EXAMINATION

When presented to our facility, the patient was bright and alert.

– The most relevant abnormalities were isolated to the upper respiratory system and included:

• Left-sided epistaxis
• Mildly decreased airflow from left nares.

– An oral examination revealed:

• Mild dental calculus with no visible evidence of mass lesions or fistulas
• Normal soft and hard palate.

– The face appeared symmetrical; the left globe retropulsed normally without evidence of discomfort.
– No pain was elicited upon palpation of the frontal sinuses and nasal planum.
– The pigment around the nares appeared normal.

DIAGNOSTICS

Laboratory Analysis

A complete blood count (CBC), serum biochemistry profile, prothrombin time (PT), and activated partial thromboplastin time (APTT) were performed by the referring veterinarian at onset of epistaxis, just prior to presentation to our facility, ruling out coagulapathies (ie, vitamin K antagonist rodenticide toxicity), polycythemia, and thrombocytopenia as causes of the epistaxis. See the Table for pertinent laboratory results.

Systolic, diastolic, and mean arterial blood pressure measured by noninvasive oscillometry were within normal reference ranges, ruling out systemic hypertension as a cause of epistaxis.
Because the patient had not traveled outside of Colorado, serum titers for infectious etiologies were likely to be low yield and were not pursued.

IMAGING

Radiography & Ultrasonography

Thoracic radiographs and abdominal ultrasound were recommended to rule out metastatic neoplasia due to the history of cough, chronic nasal discharge, acute onset of epistaxis, and elevated alkaline phosphatase.

Computed Tomography

The client elected to pursue computed tomography (CT) of the nasal cavity and sinuses and rhinoscopy. The patient was anesthetized and a CT scan of the nose and frontal sinuses was performed. The scan showed a soft tissue mass in the left nasal passage that extended from the third premolar to the rostral portion of the nasal turbinates and palate (Figure 2). The cribiform plate appeared to be intact. At this time, a presumptive diagnosis of neoplasia was made, with nasal adenocarcinoma being most likely.

Figure 2. CT scan of patient demonstrating a soft tissue mass density in the left nasal passage (arrow) and destruction of the underlying hard palate (arrowhead); note that no evidence of hard palate destruction was palpable or visible on physical examination.

Rhinoscopy & Nasal Hydropulsion

Rhinoscopy was performed with rigid and flexible endoscopes (Figure 3). A retroflexed view of the left nasal choana revealed an abnormal yellow-white, friable mass that extended rostrally from the level of the third premolar (Figure 4).

Samples of the mass were obtained with biopsy forceps and the rigid scope; then nasal hydropulsion (10 × 60 mL syringes sterile saline) was performed (Figure 5). A 4 cm × 1 cm × 1.5 cm mass was hydropulsed from the left nasal passage and retrieved from the oral cavity (Figure 6). Hemorrhage following biopsy and hydropulsion was minimal. The histopathologic evaluation revealed that the mass was a nasal carcinoma.

TREATMENT

The dog was discharged with tramadol, 100 mg (3.9 mg/kg) PO Q 8 H, and piroxicam, 7.5 mg (0.56 mg/kg) PO Q 24 H, pending results of the histopathology. Following definitive diagnosis, the clients were given an option for referral for radiation therapy, which they declined. Piroxicam was continued at the same dose. Two months later, the dog is free of clinical signs, and described by her owners to be doing well.

DISCUSSION

Epistaxis is a relatively common presenting complaint in both human and veterinary emergency rooms.² In this case report, the pet owners sought additional diagnostic tests after 5 months of recurrent and progressive nasal discharge and coughing (caused by postnasal drip related to the nasal neoplasia) and when nasal discharge progressed to stertor and epistaxis.

Epistaxis Studies

• In 1 study of epistaxis, 90/132 of dogs had local disease and the remaining 42 had systemic disease.2 Nasal neoplasia was found in 50% to 86% of cases of epistaxis that occurred in combination with at least 1 of the following other nasal abnormalities: sneezing, stertor, anatomic deformation of the nose or frontal sinus, decreased airflow, mucopurulent nasal discharge, pain, and epiphora.
• In 2 other studies, epistaxis occured in up to 75% of cases of nasal neoplasia, and the presence of epistaxis was thought by some to be reflective of a patient’s quality of life, as clients’ perceived that quality of life diminished once epistaxis occurred.^3,4
• In another study in Greece, where infectious causes of epistaxis are more prevalent than in the United States, spontaneous epistaxis in dogs was found to be more likely related to Ehrlichia and Leishmania.⁵
• In dogs older than 10 years of age (in geographic areas that do not have Ehrlichia and Leishmania) epistaxis is significantly more likely to be caused by intranasal neoplasia, compared with younger dogs.^5,6

Prognosis

The prognosis for dogs with untreated nasal carcinomas is poor.³ The results of several studies^3,7 show that median survival of:

• Dogs with nasal carcinoma was 95 days if left untreated
• Dogs with nasal adenocarcinoma and epistaxis was 88 days without treatment.

Treatment

Radiation Therapy
Radiation therapy, with or without surgical debulking (removal of as much of the tumor as possible), is considered to be the gold standard of care for dogs with nasal carcinoma. This therapy can increase the median survival of dogs with nasal carcinoma to 14 months.^8-10

Surgical Debulking
Surgical removal of large masses from the nasal cavity without additional chemotherapy and/or radiation therapy does not provide additional survival benefit because the tumor has often invaded the surrounding bone. While surgery may improve airflow through the nostrils, in some cases, radical removal of a portion or all of the nose needs to be performed to remove the tumor. Aesthetically this may be objectionable to some clients, although the patient’s quality of life does not appear to be diminished.

NSAID Therapy
Cyclooxygenase-2 (COX-2) expression has been documented in 80% of canine nasal carcinomas.^11,12 COX-2 expression has also been demonstrated in other carcinomas. In some neoplasms, COX-2 selective inhibition with piroxicam has been shown to have some efficacy for treatment (eg, transitional cell carcinoma).^13,14 However, piroxicam therapy for nasal carcinoma is considered controversial, as studies have not demonstrated improved survival with the use of piroxicam alone.³ Recent trials have been undertaken to determine whether other COX-2 inhibitors are effective in the treatment of other types of tumors in which COX-2 expression is increased, such as transitional cell carcinoma of the urinary bladder. For this reason, other COX-2 inhibitors may be effective in the treatment of nasal adenocarcinoma, and at minimum, decrease inflammation and provide palliative analgesia for patients with nasal tumors.

Nasal Hydropulsion
Nasal hydropulsion is a minimally-invasive technique recently described to debulk and collect samples from nasal tumors.¹⁵

• Forceful application of varying volumes of sterile saline were successful at debulking tumors in 90.2% of dogs and cats with nasal tumors.¹⁵
• Following successful hydropulsion, clinical signs of stertor and nasal discharge also improved in 1/3 of cases.
• This technique is also potentially useful for the treatment of nasal foreign bodies.
• Ideally, a CT scan should be performed prior to nasal hydropulsion to ensure that the cribiform plate is intact; thus, preventing adverse neurologic sequelae, such as seizures or increased intracranial pressure.

APTT = activated partial thromboplastin time;
CBC = complete blood count;
COX-2 = cyclooxygenase-2;
CT = computed tomography;
PT = prothrombin time

References

1. Gieger T, Northrup N. Clinical approach to patients with epistaxis. Comp Cont Educ Pract Vet 2004; 26:30-44.
2. Bissett SA, Drobatz KJ, McKnight A, et al. Prevalence, clinical features, and causes of epistaxis in dogs: 176 cases (1996-2001). JAVMA 2007; 231:1843-1850.
3. Rassnick KM, Goldkamp CE, Erb HN, et al. Evaluation of factors associated with survival in dogs with untreated nasal carcinomas: 139 cases (1993-2003). JAVMA 2006; 229:401-406.
4. Yasbek KV, Fantoni DT. Validity of a health-related quality-of-life scale for dogs with signs of pain secondary to cancer. JAVMA 2005; 226:1354-1358.
5. Mylonakis ME, Saridomichelakis MN, Lazaridis V, et al. A retrospective study of 61 cases of spontaneous canine epistaxis (1998- 2001). J Small Anim Pract 2008; 49:191-196.
6. Strasser JL, Hawkins EC. Clinical features of epistaxis in dogs: A retrospective study of 35 cases (1999-2002). JAAHA 2005; 41:179-184.
7. 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.
8. LaDue TA, Dodge R, Page RL, et al. Factors influencing survival after radiotherapy of nasal tumors in 130 dogs. Vet Radiol Ultrasound 1999; 40:312-317.
9. Northrup NC, Etue SM, Ruslander DM, et al. Retrospective study of orthovoltage radiation therapy for nasal tumors in 42 dogs. J Vet Intern Med 2001; 15:183-189.
10. Adams WM, Bjorling DE, McAnulty JE, et al. Outcome of accelerated radiotherapy alone or with accelerated radiotherapy followed by exteneration of the nasal cavity in dogs with intranasal neoplasia: 53 cases (1990-2002). JAVMA 2005; 227:936-941.
11. Kleiter M, Malarkey DE, Ruslander DE, et al. Expression of cyclooxygenase-2 in canine epithelial nasal tumors. Vet Radiol Ultrasound 2004; 45:255-260.
12. Borzacchiello G, Paciello O, Papparella S. Expression of cyclooxygenase-1 and -2 in canine nasal carcinomas. J Comp Pathol 2004; 131:70-76.
13. Knapp DW, Richardson RC, Chan TC, et al. Piroxicam therapy in 34 dogs with transitional cell carcinoma of the urinary bladder. J Vet Intern Med 1994; 8:273-278.
14. Correa SS, Maudlin GN, DeNicola DB, et al. Evaluation of piroxicam for the treatment of oral squamous cell carcinoma in dogs. JAVMA 2001; 218:1783-1786.
15. Ashbaugh EA, McKiernan BC, Miller CJ, et al. Nasal hydropulsion a novel tumor biopsy technique. JAAHA 2011; 47:312-316.

Elisa M. Mazzaferro, MS, DVM, PhD, Diplomate ACVECC, is the director of Emergency Services at Wheat Ridge Veterinary Specialists, in Wheat Ridge, Colorado. She is also the Scientific Program Coordinator for the International Veterinary Emergency and Critical Care Symposium (IVECCS) and the Interactive Laboratory Coordinator for the American Veterinary Medical Association’s (AVMA) annual convention. Dr. Mazzaferro’s clinical interests include trauma, pain management, and metabolic emergencies and she lectures nationally and internationally on these topics and others related to emergency and critical care medicine. She is the co-author of 2 textbooks on the subjects of emergency and critical care, editor of Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Emergency and Critical Care, and author of numerous peer-reviewed publications. Dr. Mazzaferro received her DVM from Michigan State University and her PhD from Colorado State University.