Feline Aural and Nasopharyngeal Polyps

Feline aural-nasopharyngeal polyps are non-neoplastic growths that originate from the middle ear and/or the adjacent entrance to the auditory canal. Aural polyps are those that extend from the middle ear, through the tympanum into the horizontal canal of the ear. Nasopharyngeal polyps are those that extend through the auditory canal into the posterior pharynx. Aural-nasopharyngeal polyps are the most common nasopharyngeal disease of young cats and the most common non-neoplastic mass of the feline ear [1,2].

Polyps are seen in young to middle-aged cats, with the mean age at presentation variably reported as 18 months 3-5 or 6.0 years [6,7]. The range is 3 months to 18 years [3-7]. There does not appear to be any breed or sex predisposition [3-7].

Etiopathogenesis

Polyps appear to be inflammatory or post inflammatory lesions. Histologically, the growths are characterized by loosely arranged fibrous tissue throughout which are scattered plasma cells, lymphocytes, neutrophils, lymphoid aggregates or follicles, and variable numbers of mucus-secreting glands [4,8,9]. Often, just beneath the epithelium, are focal areas of increased vascularity and, at times, heavy infiltrations of both acute and chronic inflammatory cells [8,9]. Polyps are covered by a stratified squamous to ciliated columnar epithelium that may be ulcerated [3,8,9]. The ciliated columnar epithelium cannot be differentiated from that covering the nasopharynx, auditory canal, or lining of the middle ear [10]. Grossly, polyps may be smooth or lobulated and pale pink or grey [9]. Nasopharyngeal polyps and many aural polyps are usually firm or rubbery on cut section [9]. This firmness facilitates grasping with forceps for purposes of removal by traction or avulsion. Some aural polyps tend to be more myxomatous, and friable, suggesting a shorter duration of growth [8].

The etiology of polyps remains unclear. Because the lesions have an inflammatory component, the most likely initiating cause would be irritant in nature [10]. Both viral [2,7,11] and bacterial infections [9] have been hypothesized. Support for an infectious etiology is suggested by the occasional observation of multiple, unrelated cats all developing polyps at about the same time [11].

Although reports exist of calicivirus isolation from polyp material [11,12], the incidence is low and is likely an incidental finding. In a study of 41 polyps, feline herpesvirus-1 and feline calicivirus were not found by RT-PCR and PCR [7]. The fact that the samples in this study were formalized may have contributed to some false negative results. Although this data suggests that viral persistence is not a likely cause of the problem, it does not rule out the possibility that viruses may initiate the syndrome, but are eventually cleared.

It is also possible that bacterial infection that has ascended the auditory tube may be responsible for initiating and perpetuating polyp growth [9]. Cats are prone to viral upper respiratory infections that may be complicated by secondary bacterial infection. However, most cats do not have a history of upper respiratory infections antedating polyp development [7], and the middle ear of cats with nasopharyngeal polyps are usually sterile [4]. This again does not preclude the possibility that bacterial infection may have initiated the problem.

A role for other infectious organisms such as Bartonella, Mycoplasma, and/or Chlamydia has not been evaluated to date.

Because polyps have been noted in very young individuals, it has also been hypothesized that they may be congenital defects arising from remnants of brachial arches [13]. However, no data exist to support this conjecture.

The initiating cause of polyp growth is likely no longer present at the time of clinical presentation. This is supported by the fact that relatively complete removal utilizing ventral bulla osteotomy (VBO) results in a lack of regrowth in the vast majority of cases of both aural and nasopharyngeal polyps [3,4,6,7].

Site of Origin

The middle ear of the cat is divided into a smaller dorsolateral and a larger ventromedial chamber by a thin bony plate. The dorsolateral chamber is bordered medially by the bony cochlear promontory and petrous temporal bone and laterally by the tympanum. It contains the auditory ossicles and a postganglionic sympathetic nerve plexus that fan out over its medial wall [14,15]. The communication between these chambers is limited to a narrow fissure between the bony plate and cochlear promontory on the caudomedial aspect of the compartment. Toward its caudal extremity, the fissure enlarges into a triangular foramen [14,15]. The round window of the cochlea makes up part of the medial wall of this opening. The auditory canal, which is 5 to 8 mm long [15], arises from the anterior-most aspect of the dorsolateral chamber and extends into the posterior pharynx.

Only rare reports exist of post-mortem dissection to document the site of origin of polyps. In one young cat with nasopharyngeal and middle ear polyps, the only site of attachment for both was in the region of the opening of the middle ear into the auditory canal [16]. Site of origin correlations are otherwise presumptive and based on radiographs and observations made during surgical therapy.

A middle ear site of origin for both aural and nasopharyngeal polyps is supported in the vast majority of cases by the observation that a middle ear mass is seen radiographically and by surgical exploration via ventral bulla osteotomy [4,5]. A dorsomedial chamber site of origin is supported by the observation that, during ventral bulla osteotomy in affected cats, polyps are attached to the walls of the dorsolateral compartment but not to the walls of the ventromedial chamber. Polyp growth likely extends from the dorsolateral chamber through the communicating fissure and foramen to fill the ventromedial chamber. Its growth may produce pressure necrosis of the thin bony plate that separates the chambers. This would explain the observed absence of the bony plate at the time of ventral bulla osteotomy in many patients. Nasopharyngeal polyps are occasionally seen without radiographic middle ear involvement. In these individuals, polyp growth appears to occur from around the opening to the auditory canal [4]. After traction for removal of nasophyaryngeal polyps, a stalk is seen attached to the polyp that corresponds to the approximate length of the feline auditory canal [4].

The attachment of the polyp to submucosal tissues overlying the medial bony wall of the dorsolateral chamber is further supported by the common occurrence of a transient Horner's syndrome following avulsion/traction of both aural or nasopharyngeal polyps [4,6].

Complicating Factors

Mucoid secretions are commonly noted in the middle ears of cats with middle ear polyps [14]. The epithelial lining of the middle ear contains mucus-containing goblet cells [17,18]. With chronic irritation, mucus-secreting glands are also noted to develop [17,18]. The presence of polyp material within the middle ear likely stimulates increased mucus production through irritation. It is also noted that occlusion of the auditory canal in normal cats results in the accumulation of a viscous, mucoid material which is of goblet cell and mucus gland origin [17,18]. These secretions normally exit the middle ear through the auditory canal. Polyp material partially obstructing the auditory canal likely results in mucoid-material retention in affected cats.

Secondary bacterial infections are also commonly noted in the middle ears of cats with aural polyps (17 of 22 reported cases) [5,6,19-21]. Bacteria noted (in decreasing order of frequency) include Pasteurella multocida, Beta Hemolytic Streptococcus, Staphylococcus hominis, Bacteroides sp., Pseudomonas sp., and Streptococcus zooepidemicus [6]. The incidence of secondary infections warrants the routine practice of cytologic examination and culture and the use of postoperative antibiotics in the management of aural polyps [6]. This tendency toward the development of secondary infections is likely related to perforation of the tympanum and bacterial access from the ear canals.

It is uncommon to have secondary middle ear infections in cats with nasopharyngeal polyps (3 of 23 cases in one study [4]). In these cases, the bacteria isolated included Bordetella sp., Pasteurella sp., and Achromobacter sp. Obstruction of the auditory canal is noted to predispose to secondary bacterial infection of the middle ear in the cat [17]. The middle ear of the cat has a normal, transient bacterial flora. Retained secretions associated with obstruction likely produce a microenvironment that is conducive to infection. Partial obstruction owing to nasopharyngeal growth may predispose to infection through a similar mechanism.

History and Clinical Signs

Initial clinical signs may be noted from days to years prior to presentation [3,4,7]. Polyps are most commonly unilateral at presentation. In one study of cats with only nasopharyngeal polyps 21 were unilateral, 4 were bilateral [4]. In a group with only auricular polyps, 10 were unilateral, 2 were bilateral [6].

Growth of the polyp from the middle ear is usually into the auditory canal or through the tympanum into the horizontal canal, or both. In one study of 28 cats, 50% were otic alone, 21% nasopharyngeal alone, and 29% a combination of both [7]. In another study of 37 cats, 51% had growth into the nasopharynx, 38% into the ear, and 11% of cats had both [3].

At the time of presentation, polyps have almost always extended into the horizontal ear canal or the nasopharynx. It is difficult to say what clinical signs, if any, are associated with early polyp growth confined to the middle ear. It is likely that clinical signs at this point are minimal as supported by the lack of clinical signs of otitis media (head shaking, pain on opening mouth, neurologic signs) seen in a group of individuals with only nasopharyngeal polyps and radiographic and exploratory evidence of bulla involvement [4].

The clinical signs associated with auricular polyps include debris accumulation within the ear canals, head shaking, scratching, and intermittent or consistent head tilting [6]. Intermittent head tilting is usually because of discomfort rather than neurologic dysfunction. These signs are likely products of perforation of the tympanum, irritation within the horizontal canal, and secondary bacterial and/or Malassezia colonization/infection within the canals. Debris accumulation in the canals is common and may be waxy to purulent [5]. These accumulations are a product of disruption of the normal "flushing" mechanism of the ear (lateral epithelial growth from the region of the tympanum), polyp irritation, and bacterial and/or Malassezia colonization/infection. Any source of irritation or inflammation within the ear canal results in increased ceruminous secretions. The actual incidence of bacterial and/or Malassezia colonization/infection has not been reported in affected cats; however, in the author's experience, they are common.

Neurologic signs of otitis media (Horner's syndrome, facial paresis, and paralysis) and otitis interna (head tilt, nystagmus, ataxia) are only uncommonly noted in patients with aural polyps [5,8,19]. These signs are most likely complications of secondary infections of the middle ear that could gain access to the inner ear through the membrane-covered oval or round window [19]. When infection is not present, it has been suggested that inner ear signs may be a product of increased pressure within the inner ear, mediated by pressure on the round and/or oval windows [21].

The clinical signs associated with nasopharyngeal polyps are related to progressive growth down the auditory canal, occlusion of the auditory canal, or gradual growth and expansion into the posterior pharyngeal region. Most masses are visible within the posterior pharynx at the time of clinical presentation, both clinically and radiologically (30/31 cases in one study [4]). Visualization is facilitated by forward traction on the soft palate. Clinical signs of the expanding mass in the posterior pharynx include inspiratory stridor and snoring [5], nasal discharge, gagging, and sneezing [5]. Nasal breathing may be compromised [22], and sleep may be interrupted because of a need to mouth breath. Severe obstruction may result in dyspnea, cyanosis, and syncopal collapse [15]. Breathing difficulties and/or decreased ability to smell may result in significant inappetence. Large masses may impinge on the larynx and cause voice changes and may produce dysphagia. Affected cats may want to eat, but may have difficulty in swallowing. Halitosis may be significant [3]. These various problems may produce significant weight loss and loss of general bodily condition. Affected patients are prone to the development of secondary bacterial rhinitis or sinusitis. These signs may contribute to the symptoms and may be difficult to differentiate from the signs associated with polyps. Lower respiratory tract disease (pneumonia) can develop in chronic or severe cases, likely owing to compromise of large-airway clearance mechanisms. Neurologic signs associated with nasopharyngeal polyps are uncommon (noted in 3 of 31 cases in one study [4]). These are most likely related to the development of secondary infection within the middle ear as suggested for aural polyps.

Factors Affecting Prognosis

Once polyps are clinically visible, the nature of the inflammatory process seems to make the masses relatively resistant to the effects of both anti-inflammatory and immunosuppressive dosages of oral glucocorticoids and topical glucocorticoids (for aural polyps) [8].

In those cases in which significant tissue is left within the bulla, regrowth is common [4,6,7]. In one study, mean time to regrowth was 3.5 months; range of 1 to 9 months [3]. This is most commonly noted with aural polyps treated with traction/avulsion [3,7] and is most likely related to the fact that, with this technique, significant polyp material remains within bulla. For this reason, many authors recommend VBO as the management of choice for both aural and nasopharyngeal polyps [4,7]. More recently, it has been noted that the use of a decreasing dosage regimen of oral glucocorticoids results in the lack of regrowth following partial removal via traction/avulsion of both aural and nasopharyngeal polyps [3]. Significant polyp remained within the bulla of affected patients and regrowth would have been expected in several. No regrowth was noted in 8 of 83 and 6/6 cases [23]. These observations would suggest that, even with significant polyp material left in the bulla, the creation of an acute inflammatory microenvironment through traction/avulsion allows the anti-inflammatory effects of glucocorticoids to be effective in causing residual polyp tissue to regress.