Canine Chronic Inflammatory Rhinitis

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Chronic inflammatory rhinitis is commonly found in dogs with chronic nasal disease and is characterized by lymphoplasmacytic infiltrates in the nasal mucosa in the absence of an obvious etiologic process. The pathogenesis of lymphoplasmacytic rhinitis remains unknown. Animals respond poorly to antibiotics, oral glucocorticoids, and antihistamines, making primary infectious, immune-mediated, or allergic etiologies unlikely. Aberrant immune response to inhaled organisms or allergens may induce inflammation in some animals. Common clinical signs include nasal discharge, sneezing, coughing, epistaxis, and stertor. Diagnosis is made by performing a thorough history, physical examination, radiography or advanced imaging (via computed tomography or magnetic resonance imaging), rhinoscopy, and nasal mucosal biopsy to rule out primary etiologies of nasal discharge. Treatment strategies have included various antibiotics, antihistamines, oral and inhalant steroids, nonsteroidal antiinflammatories, and antifungal medications. Some dogs may respond partially to doxycycline or azithromycin, although it is unclear whether response is related to antimicrobial or antiinflammatory properties of these drugs. Hydration of the nasal cavity through nasal drops or aerosols may limit nasal discharge, and some animals may improve with inhalant (but rarely oral) glucocorticoids.

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Etiology

The etiology of LPR has not been determined, although infectious, allergic, and immune-mediated mechanisms have been suggested. LPR may have a multifactorial etiology in some dogs and/or different etiologies in different dogs, making it difficult to develop general treatment guidelines.

History

Important historical features in dogs with chronic rhinitis include duration and progression of clinical signs, character and laterality of nasal discharge, and response to previous medical therapies. LPR can be seen in any breed but occurs most commonly in large-breed dogs. There is no apparent age or sex predilection. Duration of clinical signs may range from weeks to years at the time of diagnostic evaluation. The most common clinical signs include nasal discharge, sneezing, coughing (likely

Physical Examination

The most common physical examination findings in dogs with LPR include fresh or dry nasal discharge or crusting around the nares. Most animals have mucoid or mucopurulent discharge, but hemorrhagic or serous discharge may be seen. Nasal airflow should be assessed using a microscope slide or cotton ball wisp. When assessing the patency of airflow, each nostril should be manually occluded to watch for a stress response, indicating occluded nasal airflow in the contralateral nostril. Nasal airflow

Laboratory Evaluation

Complete blood count, chemistry panel, and urinalysis are often unremarkable in patients with chronic rhinitis. Dogs with epistaxis should be evaluated for clotting abnormalities by performing a platelet count OSPT, APTT, and BMBT to rule out coagulopathies, thrombocytopenias, and/or thrombocytopathias. Dogs presenting primarily for epistaxis should also have blood pressure measured for detection of systemic hypertension.

Imaging Techniques

Radiography has been used in some cases to help differentiate LPR from

Treatment

No effective treatment regimen for LPR has been established; therefore, animals are commonly treated with a variety of medications including antibiotics, antiinflammatory drugs (glucocorticoids: oral or topical, or nonsteroidal antiinflammatory drugs), antihistamines, and antifungal medications.

Conclusion

Inflammatory rhinitis is commonly found in dogs with chronic nasal disease. The etiology of this disorder remains unknown and may involve different pathogenic mechanisms in different dogs with chronic nasal disease. Some dogs may exhibit an aberrant immune response to commensal fungal organisms or other inhaled pathogens or irritants. The diagnosis of LPR requires a thorough history and physical examination, advanced imaging (CT or MRI), rhinoscopic evaluation, and biopsy. Culture and cytology

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    Supported in part by the Bailey Wrigley Fund and the American Kennel Club Grant 0389, and the Joseph and Mable Howe Research Scholarship.

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