Sneezing is a reflexive response to irritation of the nasal mucosa. This is a generic reaction to multiple irritant pathways that include vascular responses associated with sudden changes in ambient temperature, benign focal irritation due to small particle exposure such as dust, an attempt to clear secretions, or chronic irritation as a result of space-occupying masses.

The character of nasal discharges can vary widely. The types of discharges commonly seen are serous (clear and thin), hemorrhagic (blood tinged to frank blood), purulent (thick and cloudy), and mucoid (clear to cloudy). Purulent and mucoid discharges may appear grossly similar but can be differentiated cytologically. Mucus is normally present within the nasal passage, although the volume of mucus production can increase secondary to mucosal irritation and chronic inflammation. Inflammation results in vasodilatation and increased vascular permeability, which can result in serous, serosanguinous, or frank hemorrhagic discharge. Purulent discharge results from inflammatory reactions within the tissue that involve predominantly neutrophil extravasation.

The nasal passages are a complex matrix of turbinates and passages that serve two primary purposes, to warm and clean inspired air. Air inspired through the nose passes over a large surface area of superficial capillaries where counter-current heat exchange warms the air before it enters the lower airways. As a result of the convoluted structure of the nasal turbinates and the large mucosal surface area, increased airflow turbulence promotes large particles to settle out of the air. Mucus helps to trap these particles, which are then transported back to the nasopharynx and ultimately swallowed or removed from the nasal passage by a massive expulsion of air that constitutes a sneeze.

Many anatomical structures of the nasal passages are germane to the clinical signs expected in cases of nasal disease and will be briefly discussed. The scrolls of the turbinates (also known as choanae) are very thin and easily damaged as are the bone plates that separate the airway from the sinus cavities of the skull. Many accessory cells and tissues contribute to the proper functioning of the nasal mucosa and include mucous and serous glands within the submucosal tissue as well as goblet cells within the respiratory epithelium. The nasolacrimal duct also drains into the nasal passage and contributes to nasal discharge. The combination of ciliated respiratory epithelium and mucus from the goblet cells creates the mucociliary escalator that brings debris from the lower airway and delivers it to the pharynx. Similarly, debris from the caudal portion of the nasopharynx is moved toward the pharynx to be coughed up or swallowed. Both the curves within nasal turbinates and the decrease in airway size are essential for the removal of particulate matter from inhaled air. Air turbulence created by turbinates causes particles greater than 5 μm in diameter to impact mucosal surfaces at curves in the cartilage. As airflow slows in the lower airway secondary to the increased branching of the bronchi and bronchioles and subsequent increase in total area of passages, particles between 1 and 2 μm settle out against the airway wall (Cunningham 2002).

The response of the nasal cavity to disease is essentially limited to an increase in protective mucous secretions and the vascular responses associated with inflammation and/or infection. The end result of a prolonged or recurrent insult to the nasal cavity is loss of turbinate structure and damage to ciliated epithelium, which eliminates their function as defense mechanisms. Because of the nasal cavity’s generic response to injury, determining the specific cause of disease can be difficult and distinguishing between malignant and benign processes is not always straightforward. Due to the size and superficial nature to the nasal capillary network, inflammation can result in abundant fluid secretion by simple vascular leakage. When tissue invasion occurs, either by an infectious organism or by an infiltrative neoplasm, both vascular injury and a glandular response may occur. The two primary mechanisms to clear excess fluid from the nasal cavity are sneezing and swallowing. An increase in the volume of intranasal fluid leads to leakage from the nares. With the extensive vascular network so close to the surface of the nasal mucosa, development of a hemorrhagic component is common. Nasal hemorrhage can be severe, even life threatening, if the loss of vascular wall integrity involves large vessels within the nasal passages. This type of vascular damage is most commonly seen with invasive lesions such as fungal granulomas and neoplasms.

An important issue with nasal disease is the general irreparability of delicate intranasal structures. Thus, if the bony scrolls of nasal turbinates are destroyed by disease or if glandular hyperplasia occurs as a response to injury, the subsequent dysfunction in the system will persist even after the primary disease has resolved. One of the most common instances in which this is encountered is the destruction of nasal turbinates as a result of feline upper respiratory infections, predominantly by herpes virus and calicivirus. Even without active infection, damage to the defense mechanisms of the turbinates predisposes the animal to chronic secondary bacterial infections, which are not resolvable, due to the permanent loss of normal structural defense. In these cases, symptomatic treatment of recurrent infections becomes the only therapeutic option. The major goal in diagnosing nasal disease is distinguishing a progressive, potentially life-threatening process that demands specific medical or surgical treatment from a chronic, nonprogressive disease that will require long-term, symptomatic management.

The causes of nasal discharge and sneezing are divided into three major categories that include inflammatory, infectious, and neoplastic processes (Windsor et al. 2004; Windsor and Johnson 2006; Demko and Cohn 2007). The initial step in developing a diagnostic plan is obtaining a comprehensive history that includes any known disease, even as far back as the pediatric life stage if possible. Although owners may not always have this information, it is very helpful when available. In addition to gathering a broad, general history, specifically inquire about the nature of the clinical signs, including type of discharge as well as frequency of the clinical problem and recent changes in duration or persistence of perceived disease. In addition, note responses to previous therapy. The next step is a thorough physical examination to evaluate the overall patient and distinguish primary local nasal disease from systemic disease that is manifesting with nasal-associated clinical signs. Things that may be especially important in indicating systemic involvement include unexplained weight loss, muscle atrophy, inappetance, lethargy, changes in behavior, or changes in hair coat quality. In dogs, neoplasia, lymphoplasmacytic rhinitis, and fungal rhinitis are the most common causes of chronic nasal discharge (Windsor and Johnson 2006). In cats, the most frequent confirmed diagnosis associated with nasal discharge is neoplasia; however, a specific cause may not be identified in 1/3 of cats despite extensive diagnostic evaluation (Demko and Cohn 2007).

It is important to perform diagnostics that will localize the site of disease. Holding a hair in front of the nares or a glass slide to evaluate for condensation can help to establish unilateral or bilateral airflow obstruction. Observe for symmetry of the face, eyes, lips, and nares. Palpation of the facial tissue can help to identify the presence of a space-occupying lesion. A cranial nerve examination should be performed, as abnormalities will help to localize lesions. The presence of discharge and cytological evaluation of an impression smear or swab can help to identify cell types and microorganisms. Bacterial culture and sensitivity can be performed to aid in the management of both primary and secondary infections. Imaging studies, which can help evaluate turbinates and other osseous structures, should be done before any type of invasive nasal examination, since manual abrasion of turbinates generally causes considerable hemorrhage and will interfere with image interpretation. Because of the fine, overlapping structure of the nasal turbinates, imaging requires heavy sedation or anesthesia. Plain film radiography can identify space-occupying lesions or loss of normal turbinate structure suggestive of an invasive lesion. Computed tomography is much more effective in identifying subtle lesions and evaluating the invasiveness of a lesion (Saunders et al. 2004; Lefebvre et al. 2005; Tromblee et al. 2006). Rhinoscopy allows the visualization of the rostral portion of the nasal cavity as well as the nasopharynx and choanae. In addition, deep nasal flush can be done and samples collected for cytology and/or biopsy as well as bacterial/fungal culture and sensitivity. The depth to which the nasal cavity can be explored is dependant on the size of the patient and size of available equipment. Since rhinoscopy allows detection and visualization of focal plaques or lesions with specific sample collection from these areas of interest, the diagnostic yield of these specimens is likely to be increased. Biopsy with rhinoscopic evaluation improves diagnostic ability over visualization alone (Johnson et al. 2004).

Consider these general concepts when developing a differential list. Neoplasia is more common in mature to geriatric animals. Systemic versus focal disease should always be evaluated for at the onset, even if the owner is only aware of the single presenting problem. Foreign bodies and trauma will be more common in active pets and animals with young children in the household. Infectious diseases are more common in outdoor pets. Travel history is of great importance, especially when considering the possibility of infectious diseases that are endemic to specific regions of the country. Stress-induced onset of disease is suggestive of recrudescence of viral disease in cats. Chronic recurring bacterial infections are usually secondary and should not be treated endlessly with differing spectra of antibiotics; the primary disease should be identified whenever possible.

As previously stated, precise diagnosis in nasal disease is difficult and as many as 1/3 of cats with nasal discharge will never receive a definitive diagnosis (Demko and Cohn 2007).