Max's House

Nasopharyngeal Polyps


CHRISTOPHER L. LITTLE

Nasopharyngeal polyps are an uncommon but important cause of chronic respiratory signs in cats. Numerous reports have described the clinical presentation and management of this condition.  The condition can result in serious dyspnea and less frequently signs of aural disease, the cause of which frequently remains unrecognized. Polyps emanate from the eustachian (auditory) tube into the nasopharynx but probably have their origin in the middle ear cavity. They are composed of inflammatory granulation tissue covered by respiratory epithelium. The pathogenesis of nasopharyngeal polyps is not
known.   

PATHOGENESIS

The pathogenesis of nasopharyngeal polyps is incompletely understood. The custachian tube and middle ear cavity derive from the first pharyngeal pouch (the tubotympanic recess) and it has been proposed that nasopharyngeal polyps arise as a congenital defect of the first pharyngeal pouch. Although there is no evidence to prove this theory, the condition clearly is a disease of young cats and nasopharyngeal polyps have been reported in 2 littermates that had shown respiratory signs since shortly after birth.  An alternative theory is that nasopharyngeal polyps simply are a manifestation of chronic inflammatory middle ear disease probably caused by upper respiratory infection

The middle ear is connected to the other air spaces of the upper respiratory tract via the eustachian tube. The eustachian tube opens periodically during swallowing, yawning, and possibly at times during normal respiration, causing frequent alterations in middle ear pressure. If the eustachian tube remains closed for too long, gas in the middle ear cavity is absorbed slowly and middle ear pressure falls.  If middle ear pressure is substantially below nasopharyngeal pressure, mucus in the nasopharynx can be aspirated into the middle ear once the eustachian tube opens. However, negative pressures in the middle ear also may impair the ability of the eustachian tube to open. Upper respiratory infections can cause swelling and edema in the walls of the eustachian tube and hamper the normal function of the eustachian tube. Consequently, in a wide variety of species including the rat, rabbit, guineapig, cattle, and human being, upper respiratory infections often extend to cause otitis media. Eustachian tube dysfunction in human beings has been associated with nasopharyngeal disease such as cleft palate and rhinitis.   It has frequently been induced in cats experimentally by ligation or plugging of the tube with silastic sponges. These natural and experimental insults to the eustachian tube cause mucociliary dysfunction, hypersecretion of mucus, and otitis media with effusion, which is frequently complicated by bacterial colonization. Chronic otitis media causes inflam matory granulation tissue in the middle-ear cavity. Under these circumstances, the respiratory epithelium may undergo metaplasia from a respiratory type to stratified squamous epithelium proposes to explain the pathogenesis of feline middle ear disease and nasopharyngeal polyps based on these observations.

PATHOLOGY

The results of a postmortem examination of 1 young, cat with bilateral nasopharyngeal polyps have been reported. Each pharyngeal polyp was connected by a narrow stalk that filled the ipsilateral eustachian tube. These, stalks were continuous with polyps in the middle ear, The site of attachment on each side appeared to be in the region at which the eustachian tube opened into the middle ear.

The pathologic appearance of nasopharyngeal polyps is indistinguishable from chronically inflamed middle ear tissue They are composed of granulation tissue, which may be quite dense and mature or looser and more vascular. Blood vessels, areas of edema, and collections of inflammatory mononuclear cells frequently are found within the tissue, which also may contain primitive mucous glands. The surface of the polyp is invested either with stratified squamous nonkeratinizing epithelium or columnar respiratory epithelium that may be multilayered and ciliated in places. Goblet cells may be present within the epithe-
lium. Ulceration of the epithelial surface is common. Neutrophils and necrotic debris are sometimes present within the glands and frequently are found on the surface where ulceration has occurred. Dense lymphoid aggregates are sometimes present.


SIGNALMENT, PRESENTING SIGNS, AND CLINICAL FINDINGS

Nasopharyngeal polyps are diagnosed most frequently in young cats, with a mean age at the time of diagnosis of about 1.5 years. Nonetheless, the condition has been recognized in several cats less than 6 months of age and in cats up to 15 years of age. Similar numbers of males and females are affected. Polyps have been reported in domestic shorthair and purebred cats.

A wide variety of presenting signs have been reported in cats with nasopharyngeal polyps. The most common signs are referable to the upper respiratory tract, including noisy breathing, dyspnea, nasal discharge, sneezing, coughing, and dysphagia. Less often the presenting signs are of aural disease, typically otorrhea and aural irritation, or vestibular signs such as a head tilt. When presenting signs are referable to both the upper respiratory tract and ear, the diagnosis is straightforward . Clinical signs often have been present for many months before diagnosis.

Examination of the awake cat to confirm a suspicion of nasopharyngeal polyp is difficult. Whenever the condition is suspected, a complete physical examination should be performed. Special attention should be paid to inspection of the ears, nose, and throat; the cardiopulmonary system; and the nervous system. Horner's syndrome (miosis, ptosis, enophthalmos, and prolapse of the nictitating membrane) and vestibular signs are sometimes present. Facial nerve paralysis, while a theoretical consequence of nasopharyngeal polyps, has not been reported in affected cats prior to surgery. Confirmation of the diagnosis simply based on physical examination of the awake cat is usually impossible.

DIAGNOSIS

Examination of the oro- and nasopharynx of the anesthetized cat is the most expedient means of confinning the diagnosis. Complete airway obstruction may occur during induction of anesthesia necessitating prompt endotracheal intubation. The soft palate may bulge ventrally, and digital palpation should confirm the presence of a mass above it. The caudal edge of the soft palate can be drawn forward with tissue forceps or an atraumatic hook to allow inspection of the mass, and a dental mirror is placed within the posterior pharynx to evaluate the area above the soft palate. A flexible fiberoptic scope retroflexed 180 degrees is the most appropriate instrument to visualize this area.   Polyps appear as glistening, pedunculated, red, pink, or grayish masses occupying, and often completely filling, the nasopharynx and originating by a pedicle from either eustachian tube. Lateral radiographs of the pharynx sometimes are helpful in confirming the diagnosis but are usually unnecessary.

Complete otoscopic examination during anesthesia to evaluate both ear canals and the tympanic membranes is crucial. Most if not all cats with nasopharyngeal polyps have otitis media. Inflammatory polyps from the middle ear sometimes rupture through the tympanic membrane and grow out along the external ear canal . Otorrhea and aural irritation may be present. Radiographic examination of the middle ear is necessary, using an open-mouth projection and either a ventrodorsal or a dorsoventral view. Oblique views of the caudal skull occasionally provide additional information.  It is important to realize that radiography is not a sensitive tool in the diagnosis of otitis media. The absence of radiographic changes in the middle ear(s) does not rule out middle ear involvement. Computed tomography provides superior imaging of the middle ear and should be considered in cases in which otitis media is suspected but not documented radiographically .

Hematologic and serum biochemical values in with nasopharyngeal polyps are typically uunremarkable. Calicivirus has been isolated from 2 cases this disease, whereas in 3 other cases examined in way both calicivirus and herpesvirus were absent. A prospective study to ascertain the prevalence of th respiratory pathogens may help clarify the role, if an they play in the etiology of the disease. Isolated testing of individuals is unlikely to influence management.

TREATMENT

Surgical extirpation is the therapy of choice. Remov, of the nasopharyngeal polyp usually is easily accoplished while the cat is anesthetized by grasping with forceps and applying slow steady traction. During this task, the pedicle may be seen emerging from the eustachian tube. Postoperative hemorrhage into the nasopharynx is minimal and easily controlled by packing swabs into the nasopharynx for a few minutes. The polyp occasionally cannot be removed in this way without incisi the free caudal border of the soft palate to improve access.  The soft palate is closed in 2 layers using an absorbable material such as Vicryl. When a polyp is removed from the nasopharynx by traction, the pedicle usually is found to be 5 to 10 mm long, sufficient to indicate that the mass probably arose in the middle ear.

Controversy surrounds the issue of bulla osteotomy in cats with nasopharyngeal polyps. Ventral bulla osteotomy is associated with a high risk of complications.  It has been argued therefore that when there is no radiographic evidence of middle ear disease, bulla osteotomy is unnecessary.  However, when bulla osteotomy is not performed, recurrence of nasopharyngeal polyps is quite frequent; whereas, recurrence is rare if bulla osteotomy is performed. Therefore, some surgeons recommend that bulla osteotomy be performed on the ipsilateral middle ear of every cat with a nasopharyngeal polyp. Cats with unilateral nasopharyngeal polyps may have bilateral otitis media. Bilateral polyps have been reported.

Bulla osteotomy is performed utilizing a ventral approach with the cat in dorsal recumbency. The tympanic bulla can be palpated easily on the caudoventral skull as a bony blister lateral to the larynx and medial to the mandible. The skin and subcutis are incised; and using blunt dissection, the bulla is exposed. Avoid traumatizing the hypoglossal nerve and internal carotid artery. An osteotome or fine bone forceps is used to create a window in the tympanic bulla. This will open into
the larger ventromedial and caudal compartment, exposing the septum that divides the middle ear. Creating an opening in the septum provides access to the smaller dorsolateral compartment which contains the ossicles. Care should be taken to avoid traumatizing the promontory. The dorsolateral compartment lies rostrally and is believed by most observers to be the site of origin of nasopharyngeal. The middle ear is then curetted, but with discretion to avoid damage to the ossicles, the inner ear, the tympanic membrane, and the various nerves that pass through this location . The smaller cavity usually contains dense granulation tissue, whereas the larger ventromedial compartment more frequently contains thick tenacious mucus. A drain may be placed in the bulla for a few days after surgery. Removal of polyps from the nasopharynx by traction alone often causes ipsilateral postoperative Horner's syndrome     This observation suggests that the middle ear has been traumatized. Horner's syndrome usually resolves within I to 3 weeks. Other complications following removal of nasopharyngeal polyps by traction alone include abscess formation and cardiorespiratory arrest associated. with induction or recovery from anesthesia in 2 cats. 1 One author has described removing nasopharyngeal polyps from 8 cats by severing the pedicle of the polyp at the nasopharyngeal ostium of the eustachian tube. Postoperative Horner's syndrome was not observed in these cases.

When bulla osteotomy has been performed in the treatment of nasopharyngeal polyps, temporary postoperative Horner's syndrome developed in the majority of cases.   Ventral bulla osteotomy in cats has been associated with temporary or permanent vestibular signs, including head tilt, nystagmus, and ataxia.  Infrequently, the facial nerve may be paralyzed after surgery, leading to drooping of the lip, drooling of saliva, and lack of a palpebral reflex. This neuropathy resolves in most cases.

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