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.