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Inflammatory polyps and aural neoplasia

Article  in  Veterinary Clinics of North America Small Animal Practice · April 2004

DOI: 10.1016/j.cvsm.2003.10.008 · Source: PubMed

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 Vet Clin Small Anim
34 (2004) 489–509

Inflammatory polyps and aural neoplasia

Timothy M. Fan, DVM*,
Louis-Philippe de Lorimier, DVM
Department of Veterinary Clinical Medicine, Veterinary Teaching Hospital, University of
Illinois, 1008 West Hazelwood Drive, Urbana, IL 61802, USA

Despite the prevalence of ear diseases in companion animals, aural tumors

comprise only a small percentage of ear disorders. The development of cancer
is preceded by the malignant transformation of normal resident cells.
Therefore, ear tumors arise from normal auricular structures involved in the
protection, support, and lining of the ear canal, which include the pinnae, the
external auditory canal, the middle ear, and the inner ear. Tumors involving
the pinnae and external auditory canal are more common than tumors of the
middle and inner ear. Epithelial and adnexal cell types susceptible to neo-
plastic transformation include connective tissue mast cells, melanocytes,
squamous epithelial cells, basal cells, cutaneous plasma cells, histiocytes, and
ceruminous and sebaceous acinar cells. Additionally, mesenchymal cells,
such as fibroblasts, chondrocytes, myocytes, and vascular endothelial cells,
may give rise to cancer formation.
Aural tumors in the dog and cat can be histologically benign or malignant.
Benign aural conditions include inflammatory polyps, basal cell tumors,
papillomas, histiocytomas, and ceruminous gland adenomas. Although both
dogs and cats are susceptible to developing aural tumors, biologically, these
cancers tend to be more aggressive in the cat. Malignant aural tumors may
possess an aggressive phenotype allowing for rapid local tissue invasion,
early lymphatic spread, and distant metastasis. The most commonly reported
aural tumors affecting dogs include ceruminous gland adenoma and
adenocarcinoma, papilloma, and histiocytoma. In the cat, ceruminous gland
adenoma and adenocarcinoma are also common, but unlike the dog, cats are
more frequently diagnosed with inflammatory polyps involving the middle
ear and squamous cell carcinoma (SCC) of the pinnae.

* Corresponding author.
E-mail address: t-fan@uiuc.edu (T.M. Fan).

0195-5616/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.cvsm.2003.10.008
490 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

Feline tumors of the pinna

Squamous cell carcinoma
SCC is a cutaneous malignancy associated with increased exposure to
sunlight. In geographic regions receiving high levels of annual solar
radiation, the incidence of cutaneous SCC has been reported to be 26.9
cases per 100,000 cats [1]. Cutaneous SCC arises most commonly in areas of
poor pigmentation, with white cats having a 13.4 times greater risk of
developing SCC than colored cats [1]. In accordance with ultraviolet-
induced DNA damage resulting in SCC initiation, anatomic regions exposed
to direct sunlight, such as the nasal planum, periocular regions, and pinnae
of cats, are the most commonly reported sites of tumor development. SCC
can also develop at the base of the ear or in the preaural area of lightly
pigmented cats (Fig. 1).
Although physical carcinogenesis in the form of ultraviolet radiation has
been incriminated in cutaneous SCC development, the role of biologic
carcinogens in SCC tumorigenesis remains poorly defined. Unlike the direct
causal relation between feline leukemia virus (FeLV) and feline immuno-
deficiency virus (FIV) infections with the development of feline lymphoma,
no definitive association between feline retroviral infections and the
development of cutaneous SCC has been reported [2,3]. More than likely,
concurrent retroviral infection and sunlight-induced SCC is an epiphenom-

Fig. 1. Invasive squamous cell carcinoma of the base of the ear in a white cat.
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 491

enon associated with an outdoor population of cats at higher risk for solar
radiation exposure and contact with other free-roaming retroviral-infected
felines.

Molecular biology
The process of carcinogenesis is complex, requiring the dysregulation of
multiple genetic safeguards. Classically, malignant transformation occurs
when normal somatic cells acquire growth signal autonomy, insensitivity to
antigrowth signals, and resistance to apoptosis [4]. The acquisition of these
cellular derangements has been coined the ‘‘hallmarks of cancer.’’ In-
sensitivity to antigrowth signals may be caused by mutations in tumor
suppressor genes, such as p53. Mutations in the p53 gene are the most
frequent alteration identified in human malignancies. In the veterinary
literature, mutant p53 has been identified in various feline tumor types,
including lymphosarcoma, mammary carcinoma, osteosarcoma, fibrosar-
coma, malignant histiocytoma, basal cell tumors, and other undifferentiated
sarcomas and carcinomas [5–10]. The identification of mutant p53 in feline
cutaneous SCC has also been demonstrated by immunohistochemical
staining methodologies using reactive polyclonal antibodies (CM-1 or pAb-
240) or by gene sequencing [10–15]. At least two veterinary reports describe
p53 mutations in feline cutaneous SCC arising from the ear pinna [11,12]. In
one study, 9 of 11 cats (81.8%) with pinnal SCC had mutations in p53 [12].
Similarly, in a second study, 2 of 4 cats (50%) with pinnal SCC were
identified to have p53 protein alterations [11]. The identification of mutant
p53 in feline premalignant actinic keratosis and pinnal SCC closely parallels
the multistep transformation and development of cutaneous SCC in human
beings after chronic ultraviolet radiation exposure [14,16].

Biologic behavior
Pinnal SCC typically involves the ear tips in older white-haired cats
exposed to prolonged periods of direct sunlight. Premalignant lesions may
appear as areas of hyperemia but may eventually become erythematous,
crusty, and ulcerative. Histologically, premalignant lesions, termed actinic
keratosis, are composed of reactive proliferating keratinocytes that
eventually invade into the underlying dermis. With the accumulation of
DNA damage secondary to long-term ultraviolet radiation exposure, actinic
keratosis may acquire more invasive properties, ultimately progressing to
SCC. Pinnal SCC is considered to be a locally aggressive epithelial neoplasm
with an extremely low metastatic rate [3]. Although the ear tips of cats are
predisposed to the development of cutaneous SCC, it has been reported that
approximately 15% of cats have multicentric disease manifesting with
multiple SCC lesions involving different cutaneous locations, including the
nasal planum and conjunctival margins [17]. Infrequently, anaplastic or
undifferentiated pinnal SCC may possess a metastatic phenotype, allowing
492 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

for early neoplastic spread to regional lymph nodes or distant pulmonary

sites [18,19].

Therapeutic modalities
Given the regionally invasive nature of pinnal SCC in conjunction with
its relatively low metastatic rate, aggressive and early local therapies are
often curative. Local treatment options reported for pinnal SCC include
surgical resection, cryosurgery, and photodynamic therapy. For cats with
more aggressive or advanced disease, anecdotal evidence suggests that
adjunctive treatment options, including systemic chemotherapy and non-
cytotoxic differentiating agents, may provide marginal improvements in
disease-free interval and survival times [20,21].

Surgical resection. Pinnectomy is the most common and effective treatment

option for regionally confined SCC. When possible, wide surgical excision
should be attempted. Resected samples should be submitted for histologic
evaluation to determine if tumor-free margins were achieved. The non-
complex nature of pinnal amputation, allowance for surgical margin
evaluation, and acceptable cosmetic results make pinnectomy the best local
treatment option. In one study, amputation of the affected pinna provided
excellent disease-free and survival times (681 and 799 days, respectively). All
cats (n = 18) undergoing pinnectomy were cured of their disease, with none
of the cats experiencing local tumor regrowth [3].

Cryosurgery. Cryosurgery may be considered a reasonable treatment option

when pinnectomy is not anatomically possible or if owners would be
dissatisfied with the cosmetic effects of pinnal amputation. Cryosurgery has
similar advantages to traditional surgery, such as minimal specialized
equipment costs and availability; however, cryosurgery does not allow for
surgical margin assessment. Because the effectiveness of cryosurgery
depends on the direct freezing of abnormal tissues, its use is restricted to
superficial, small (less than 5-mm diameter), and noninvasive lesions of the
pinna. In one study, cryosurgery was extremely effective for the treatment of
cutaneous SCC arising from the pinna and eyelid margins. All cats (n = 12)
with either pinna or eyelid margin SCC achieved complete remission
subsequent to only one treatment cycle of cryosurgery. In the same study,
cats with SCC involving the nasal planum (n = 90) did not respond as well,
with approximately 20% of these cats being classified as treatment failures
[22]. The discrepant response rates between nasal planum and pinnal SCC to
cryosurgery further support the recommended use of cryosurgery only in
anatomic sites where thorough tissue freezing is achievable.

Photodynamic therapy. Photodynamic therapy (PDT) is a local treatment

modality that possesses selective tumoricidal effects and has been evaluated
in feline pinnal SCC. PDT involves the administration of a photosensitizing
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 493

agent that is preferentially retained by neoplastic tissue. Most photosensitiz-

ing agents are administered systemically as intravenous injections; however,
some agents, such as 5-aminolaevulinic acid, can be applied topically. The
localized photosensitizing agent is activated when it absorbs light of an
appropriate wavelength. On activation, the photosensitizing agent interacts
with oxygen, with the subsequent formation of cytotoxic free radicals. The
use of a light-emitting diode source allows the operator to control the
activation of the photosensitizing agent to specific regions of interest.
Clinical response to PDT therapy is dependent on the type of photo-
sensitizing agent, tumor/normal tissue photosensitizer ratio, and energy
dose delivered to the target tissues. Cats being treated with PDT must avoid
exposure to sunlight after photosensitizing agent administration to prevent
generalized cutaneous photosensitization. Adverse side effects associated
with accidental cutaneous photosensitization include depression, facial
edema, and blistering and ulceration of nonpigmented and poorly haired
areas of the skin. The effective use of PDT is restricted to superficial tumors
because of the limited penetration of light required to activate the
photosensitizing agent.
In one study using aluminum phthalocyanine tetrasulfhonate as an
intravenously administered photosensitizer, PDT was successful in treating
three cats with pinnal SCC after one treatment cycle. Despite excellent
response rates (100%), all three cats experienced tumor regrowth within 18
months of initial PDT [23]. Similarly, in a second study also evaluating
aluminum phthalocyanine tetrasulfhonate as a photosensitizer, one com-
plete response and one partial response were achieved for the treatment of
pinnal SCC in two cats. The duration of response was disappointing, lasting
only 151 and 61 days, respectively [24]. Finally, there has been one report
describing the use of topical 5-aminolaevulinic acid as a photosensitizing
agent in cats (n = 11) with superficial SCC. One cat in this study had
bilateral pinnal SCC and achieved a partial response in the left pinna and
a complete response in the right pinna. The duration of complete response
for the right pinna was at least 20 weeks [25].

Local current field radiofrequency hyperthermia. Regional hyperthermia has

been used for the treatment of large nonresectable tumors in human beings.
Besides possessing direct cytotoxic effects, hyperthermia enhances the
anticancer effects of radiation therapy, chemotherapy, and immunotherapy.
Regional temperatures exceeding 42 C are capable of causing localized cell
death within minutes [26]. Several methods have been described for
achieving regional hyperthermia, including the use of radiofrequency
currents [27]. The passage of radiofrequency currents between two electro-
des allows for the controlled delivery of heat to a target site. Radio-
frequency-induced hyperthermia has been used to treat cutaneous SCC in
the cat. Superficial lesions involving the pinna and nasal planum responded
494 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

the best to regional hyperthermia, with a reported complete response rate

for treated cutaneous SCC of 68% [28].

Additional therapies. Given that aggressive surgical pinnectomy provides

excellent disease-free and survival times, the use of adjunctive therapies for
pinnal SCC is often unnecessary. Several additional adjunctive therapies
used for the management of nonresectable SCC involving the nasal planum
have been reported, however, and theoretically may be useful for the
treatment of locally invasive pinnal SCC. In one case report, repeated laser
surgery using a neodymium:yttrium aluminum garnet (Nd:YAG) laser has
been demonstrated to be effective in controlling local disease in one cat with
nasal planum SCC [29].
The use of various forms of radiation therapy has been reported for the
treatment of cutaneous SCC. In one study using orthovoltage radiation
therapy, 90 cats with nasal planum SCC were treated with a total dose of
40 Gy administered in 10 fractions of 4 Gy over 3.5 weeks. The median
disease-free interval achieved with this radiation protocol was 16.5 months
[30]. In a smaller study, 11 cats with nasal planum SCC were treated with
megavoltage radiation (Cobalt-60), with an average dose of 45.9 Gy. The
achieved median disease-free interval and survival time were 361 and 383
days, respectively [3]. In a recent study evaluating proton beam radiation, 15
cats were treated for SCC of the nasal planum. Response rates achieved with
proton beam radiation were good, with 93% (14/15) of cats achieving
a clinical response (complete response and partial response). The median
survival time achieved with proton beam radiation was impressive at 946
days [31]. Additionally, radiation brachytherapy delivered via a strontium-
90 probe for the treatment of small noninvasive nasal planum SCC has been
described. With the use of strontium-90, nasal planum SCC was effectively
treated in 25 cats, with 89% of cats being free of disease at 1 year and 82%
of cats being free of disease at 3 years [32].
Although chemotherapy is classically considered a systemic treatment
option, the combination of cytotoxic agents with depot substances allows for
the delivery and retention of drugs to a specific area. This local therapeutic
modality is termed intralesional chemotherapy, and it has been used with
some success with nonresectable cutaneous SCC. Because cytotoxic agents
are localized and retained in a defined region, systemic toxicity is rarely
a complication and high concentrations of chemotherapy can be achieved
locally. Chemotherapeutic agents that have been evaluated in the cat include
cisplatin, 5-fluorouracil, and carboplatin. Complete response rates to
intralesional chemotherapy are good, ranging from 64% to 73.3% [33–35].

Miscellaneous tumors of the feline pinna

Although SCC comprises most feline pinnal tumors, malignant trans-
formation of other cell types that cover or provide structural support to the
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 495

pinna may occur. Pinnal tumors may arise from haired or nonhaired
epithelium as well as from mesenchymal cells that provide rigidity and
nutrients to the ear pinna. Biologically, most of the miscellaneous feline
pinnal tumors are locally invasive with a low metastatic potential, and early
surgical resection is often curative.
Rhabdomyoma is a benign mesenchymal neoplasm arising from striated
skeletal muscle. Because one of the functions of the pinna is to facilitate the
localization of sound, voluntary movement of the pinna is mediated by the
coordinated contraction and relaxation of myocytes within the pinna. One
report describes four cats with rhabdomyoma of the pinna [36]. All four cats
had white ears; however, chronic exposure to solar radiation resulting
in DNA damage could not be concluded as a causative factor. Pinnal
amputation was curative in all four cats, paralleling the expected benign
phenotype of rhabdomyomas arising from other anatomic sites.
Fibrosarcoma is a soft tissue sarcoma in the cat and accounted for 15%
of all feline cutaneous neoplasms in one study [37]. Anatomic areas most
commonly involved with fibrosarcoma development have been reported to
be the head and distal extremities [38]. Biologically, most nonvaccine-
associated fibrosarcomas are locally invasive and possess a low metastatic
potential [39]. In rare instances, aggressive fibrosarcomas may spread to
regional lymph nodes or distant sites. Limited prognostic and treatment
information exists for fibrosarcomas involving the ear pinna. In one study,
four cats with pinnal fibrosarcoma were cured of their disease after surgical
amputation of the affected ear [40]. Given the low metastatic rate of
spontaneous fibrosarcomas, aggressive and early pinnectomy should
generally provide excellent long-term results.
Vascular neoplasia accounts for a small percentage of skin tumors in
cats, with most tumors arising from the inguinal subcutis [41]. An
additional anatomic site where cutaneous vascular neoplasms may arise
in cats is the ear pinna. In one report, five cutaneous vascular pinnal
neoplasms, one hemangioma, and four hemangiosarcomas were diagnosed
and surgically excised from five cats. Tumor regrowth occurred in all
cats with hemangiosarcoma, with a median disease-free interval time of
9.5 months [42]. The incidence of metastatic disease was not able to be
determined in this study. Interestingly, all four pinnal hemangiosarcomas
developed in cats with white coat colors, potentially incriminating the role
of solar irradiation as a causative factor. Supporting the contention for
ultraviolet radiation–induced pinnal vascular tumors, chronic exposure
to sunlight has been associated with cutaneous vascular tumorigenesis in
dogs [43].
Melanomas are tumors arising from melanocytes and melanoblasts and
are the most common tumors involving the uveal structures of the feline eye.
Although uveal melanomas are common ocular tumors, the reported
incidence of nonocular dermal melanomas is low in comparison. The
biologic behavior and prognostic factors associated with nonocular dermal
496 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

melanomas have been evaluated in one retrospective study with 23 cats [44].
In this study, 4 cats with dermal melanoma arising from the pinna were
treated with wide surgical excision of the tumor. Three cats were cured of
their melanoma, but 1 cat experienced tumor regrowth and metastasis to the
regional lymph node. The conclusions drawn from this retrospective study
as well as from a larger study [37] support the notion that most pinnal
melanomas behave in a benign fashion. Nevertheless, a subset of dermal
melanomas may possess a more aggressive phenotype, resulting in recurrent
disease and early regional lymph node metastasis.
Tumors arising from uncommitted basal reserve cells of the epidermis and
adnexa include basal cell epithelioma and basal cell carcinoma. Generally,
these tumors possess a benign phenotype and are collectively termed basal
cell tumors. In the cat, basal cell tumors are the most common cutaneous
neoplasms, typically affecting the head and neck regions [37]. Because of their
pigmentation, basal cell tumors can be grossly mistaken for cutaneous
melanomas. In general, basal cell tumors involving the ear pinna can be
cured with surgical resection. A benign phenotype is not absolute; despite
aggressive pinnectomy, some tumors may invade adjacent structures and
demonstrate early lymphatic and vascular invasion [45].
Mast cell tumors are the second most commonly diagnosed cutaneous
tumor in the cat [37]. As a breed, Siamese cats are overrepresented. Feline
mast cell tumors involving the pinna have been described and account for
59% of all cutaneous mast cell tumors arising from the head region [37].
Despite the prevalence of feline cutaneous mast cell tumors, they behave in
a benign fashion [46,47]. Surprisingly, tumors incompletely excised are not
associated with a higher recurrence rate when compared with completely
resected mast cell tumors, underscoring the benign behavior of these
common skin tumors [46].

Canine tumors of the pinna

Unlike the case in cats, in which most pinnal neoplasms are SCC, tumor
types affecting the canine pinna occur with more equal frequency. Some of
the cutaneous tumors affecting the canine pinna include mast cell tumors,
histiocytomas, sebaceous gland tumors, fibromas, plasmacytomas, and soft
tissue sarcomas. Similar to their feline counterpart, the effective treatment
for most canine pinnal tumors relies on early and aggressive surgical
resection. As expected, early pinnal amputation in tumor-bearing dogs may
be curative or at least provide durable disease-free intervals. Infrequently,
canine pinnal tumors can possess metastatic phenotypes precluding the use
of only surgical excision as a curative therapeutic modality. As with any
invasive or metastatic tumor type, adjunctive therapies, such as radiation
therapy and systemic chemotherapy, may be required to maximize treatment
success.
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 497

Cutaneous aural mast cell tumors

Cutaneous mast cell tumors are the most common malignant skin tumor
affecting the dog (Fig. 2) [38]. The biologic behavior of cutaneous mast cell
tumors may be difficult to predict, delaying the institution of appropriate
therapeutics. Several predictive factors have been identified to facilitate the
accurate and reliable prognostication of cutaneous mast cell tumors.
Anecdotally, tumor location has been suggested to influence cutaneous
mast cell behavior. Mast cell tumors arising from ‘‘unfavorable sites,’’ such
as the oral cavity or mucocutaneous junctions, are believed to possess more
aggressive phenotypes [48]. Similarly, preliminary information from one
retrospective study would suggest that mast cell tumors arising from the ear
pinna or auricular flap behave aggressively. In this retrospective study of 24
cutaneous aural mast cell tumors, the incidence of regional lymph node
metastasis was reported to be 42.8% [49]. Given this relatively high
metastatic rate, to maximize response rates and survival times, the use of
adjunctive therapies would be recommended for the treatment of cutaneous
aural mast cell tumors.

Cutaneous histiocytoma
Histiocytomas are common skin tumors usually arising in young dogs.
These tumors express cluster-of-differentiation markers consistent with
epidermotropic Langerhans cells [50]. Histiocytomas usually are

Fig. 2. Recurrence of grade III mast cell tumors at the margin of a previously excised distal ear
pinna in a Springer Spaniel.
498 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

fast-growing, solitary, ‘‘button-like’’ lesions that may regress spontaneously

via immunologic recognition by CD8+ ab T cells. It has been hypothesized
that the high expression of major histocompatibility complex class II (MHC
II) on the surface of neoplastic histiocytes may play a decisive factor for
immune-mediated regression [51]. Given that many histiocytomas sponta-
neously regress, treatment for pinnal histiocytomas may include benign
neglect, conservative surgical resection, or cryosurgery. For dogs with
multiple or diffuse cutaneous involvement of the ear pinna or other
anatomic sites, the use of systemic corticosteroids or azathioprine has been
reported for the effective regression of histiocytic lesions [38,52].

Sebaceous gland tumors

Sebaceous gland tumors are a collection of four distinct histologic
subtypes, including sebaceous hyperplasia, sebaceous epithelioma, seba-
ceous adenoma, and sebaceous adenocarcinoma. Typically, sebaceous gland
tumors appear as solitary cauliflower-like cutaneous masses with a greasy
appearance and texture. Surgical excision of sebaceous hyperplasia,
epithelioma, and adenoma is often curative, with tumor regrowth rarely
occurring [53,54]. Sebaceous adenocarcinomas tend to be more invasive and
metastatic, often requiring more aggressive surgical resection and the
implementation of adjunctive therapies [55].

Tumors of the external ear canal: dog and cat

Tumors of the ear canal are relatively uncommon and may be
phenotypically benign or malignant. According to one large retrospective
study, most (87.5%) ear canal tumors diagnosed in cats are malignant, often
being carcinomas arising from the epithelial and adnexal structures of the
auditory meatus [56]. Ceruminous gland adenocarcinoma is the most
commonly diagnosed malignant feline tumor, but SCC, sebaceous gland
adenocarcinoma, and carcinoma of undetermined origin also occur with
some frequency. In dogs, the ratio between benign and malignant tumors is
more evenly distributed, with benign tumors accounting for approximately
40% of ear canal tumors [56]. Benign ear canal tumors in the dog include
papilloma, sebaceous gland adenoma, basal cell tumor, ceruminous gland
adenoma, histiocytoma, and others. Malignant canine ear canal tumors are
predominantly carcinomas arising from the ceruminous gland or squamous
epithelium or are of undetermined origin. Malignant mesenchymal cell
tumors, including invasive soft tissue sarcomas and melanomas, make up
a small fraction of aggressive tumors affecting the canine ear canal.
Similar to pinnal tumors, the effective treatment of ear canal tumors in
the dog and cat relies on complete surgical excision. As a result of anatomic
constraints, complete surgical resection of ear canal tumors may be
challenging and, in some situations, unachievable. Conservative surgical
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 499

approaches, such as lateral ear canal resection, for the treatment of ear canal
tumors often fail to provide clean surgical margins, resulting in early tumor
regrowth. With more radical surgical techniques, including total ear canal
ablative surgeries and bulla osteotomy, regional disease control can be
routinely achieved. In rare instances where ear canal tumors invade adjacent
soft tissues or metastasize to regional lymph nodes, the use of adjunctive
therapies should be considered to maximize disease-free intervals and
overall survival times.

Ceruminous gland tumors

Ceruminous glands are modified apocrine sweat glands that underlie the
superficial epithelial lining of the external ear canal. The secretory products
of ceruminous and sebaceous glands mix with desquamated keratinized
debris to make up earwax. Ceruminous gland tumors account for most
neoplasms arising from the external ear canal and include ceruminous gland
adenomas and adenocarcinomas. In dogs and cats, malignant adenocarci-
nomas are more common than benign adenomas [57]. Biologically, most
ceruminous gland tumors possess regionally invasive properties. Neverthe-
less, adenocarcinomas, especially in cats, are believed to behave more
aggressively than adenomas, with greater soft tissue infiltration and the
potential for metastasis to regional lymph nodes and distant sites [58].
Surgical excision of canine and feline ceruminous gland tumors remains
the cornerstone of therapy. In one small retrospective study, canine
adenocarcinoma treated with total ear canal ablation and lateral bulla
osteotomy was curative in seven dogs. In the same study, however, in dogs
treated with more conservative lateral ear canal resection (n = 4), local
tumor recurrence occurred in 75% of patients [59]. In a similar study, 22
cats with ceruminous gland adenocarcinoma were treated with either total
ear canal ablation with lateral bulla osteotomy (n = 16) or lateral ear canal
resection (n = 6). The 16 cats treated with more aggressive and extensive
surgical resection achieved a median disease-free interval of 42 months and
a recurrence rate of 25%. In the 6 cats treated with only lateral ear canal
resection, local disease control was disappointing, with a median disease-
free interval of only 10 months and a recurrence rate of 66.7% [60]. The
results of these two retrospective studies support the recommendations for
aggressive and extensive surgical intervention in dogs and cats with
ceruminous gland adenocarcinomas.
Although radical surgical approaches offer the best chance for local
disease control, a subset of patients with extremely invasive or metastatic
tumors cannot be effectively managed with surgery alone. Little information
exists describing the adjuvant use of megavoltage radiation therapy for the
treatment of canine and feline ceruminous gland adenocarcinomas. One
study describes the use of radiation therapy for the management of
ceruminous gland carcinomas in five dogs and six cats. A total dose of 48 Gy
500 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

was administered, and its effectiveness was assessed in a microscopic and

macroscopic disease setting. Radiation therapy was curative in four patients;
however, local tumor regrowth (n = 4) and metastatic disease (n = 3) were
the ultimate outcomes in the remaining seven patients [61]. Based on this
small cohort study, the use of radiation therapy for the management of
microscopic residual disease warrants additional investigations.

Inflammatory polyps
Feline inflammatory polyps
Inflammatory polyps, also called nasopharyngeal polyps, respiratory
tract polyps, pharyngeal polyps, or middle ear polyps, are nonneoplastic
inflammatory lesions that arise from the mucosal lining of the middle ear,
Eustachian tube, or pharynx [62–77]. Although most reports generally
describe them as being infrequently observed, they are the most common
benign pharyngeal and external ear canal masses diagnosed in cats
[62,64,66–70,72,77]. Histopathologically, inflammatory polyps consist of
loose fibrovascular tissue covered by an epithelial layer (stratified squamous
or ciliated columnar) and accompanied by mixed inflammatory infiltrates
(lymphocytes, plasma cells, macrophages, and occasionally neutrophils)
[62,64–68,71,72,78,79]. The polypoid mass can either extend through the
Eustachian tube into the pharynx and nasopharynx or through the tympanic
membrane into the external ear canal.
The exact etiology of inflammatory polyps remains unknown. Proposed
causes include a congenital origin, chronic upper respiratory tract in-
flammation, chronic otitis media, or ascending infection from the nasophar-
ynx [62,65,67–69,72,80]. Although two studies recovered feline calicivirus
from the polyps of some affected cats, a group of investigators recently
evaluated 28 patients with feline inflammatory polyps using polymerase
chain reaction (PCR) and reverse transcriptase PCR (RT-PCR) to detect
feline herpesvirus-1 and calicivirus, respectively, and obtained different
results [69,71,75]. The investigators of the latter study failed to detect viruses
in 41 polyps, suggesting that tissue persistence of calicivirus or feline
herpesvirus-1 is not a mandatory prelude to the development of feline
inflammatory polyps, although immunologic clearance of these viral
organisms before polyp diagnosis remains a possibility [75].
The typical presentation is that of a cat generally younger than 3 years of
age (reported range varies from a few weeks to 18 years of age, with a mean
age of about 24 months) with upper respiratory signs, such as nasal
discharge, sneezing, stertor, voice change, dyspnea, and dysphagia when the
mass is located in the nasopharynx; signs of otitis media/interna, such as
head tilt, loss of balance, nystagmus, and Horner’s syndrome when the mass
is in the tympanic cavity; or signs of an external ear canal mass, such as
otorrhea, head shaking, and a visible mass when the polyp protrudes
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 501

through the tympanic membrane [62–64,66–69,71,72,75,77–81]. Although

they are more frequently unilateral, it is not uncommon to find bilateral
involvement with feline nasopharyngeal polyps [62–64,66,67,75,78]. Abyssi-
nian cats may be overrepresented [62,64,67,69,72,75,79].
Diagnosis is generally obtained with a combination of signalment, history
and clinical signs, palpation of the soft palate, visual observation of a mass
(otoscopic or oropharyngeal examination), skull radiographs, advanced
imaging (CT, MRI), and histopathology (Figs. 3 and 4) [62–75,77,78,82].
Good-quality radiographs or advanced sectional imaging (CT, MRI) can
help to determine the involvement of the middle ear, which is important for
therapeutic planning [62–75,78,82]. Advanced imaging has the advantages
of improved detail and sensitivity over radiographs for detecting the extent
of osseous (CT) and soft tissue (CT and MRI) changes, making earlier
recognition of middle ear involvement possible (see Fig. 4) [73,82]. A study
showed that CT evaluation helped to determine the location of the polyps in
all three cats reported [73]. The main disadvantages of advanced imaging are
the necessity for longer anesthesia time and the increased cost.
Simple traction avulsion through the mouth or the ear canal is generally
recognized as sufficient when no middle ear involvement is present [62–
72,74,75,83]. Although it is associated with a lower recurrence rate, ventral
bulla osteotomy, with or without ear canal ablation, is typically recom-
mended only when evidence of tympanic cavity involvement is observed
on imaging because of the reported higher risk for complications [62–72,

Fig. 3. Video-otoscopic view of a feline inflammatory polyp in the external ear canal. (Courtesy
of J.L. Matousek, DVM, Urbana, IL.)
502 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

Fig. 4. CT imaging of a feline inflammatory polyp. Evidence of middle ear involvement is

confirmed by the soft tissue opacity in the ventromedial and dorsolateral compartments of the
right tympanic bulla and the accompanying severely sclerotic bone. A soft tissue opacity is also
observed filling the external ear canal (arrows). (Courtesy of S.C. Kennedy, DVM, Urbana, IL.)

74–76,78,83]. Some authors nonetheless recommend bulla osteotomy in all

patients with inflammatory polyps, with tympanic cavity involvement being
the rule in most of them, whereas others argue to treat with simple traction
initially and reserve bulla osteotomy only for recurring cases [62–64,
66,75,83]. These surgical techniques have been described elsewhere and
are discussed in another article in this issue [65,67,68,70–72,76,83]. Because
secondary otitis media is a common accompanying problem, bacterial culture
and sensitivity should be performed, with appropriate antibiotic therapy
instituted based on the results obtained.
The main complication observed after bulla osteotomy is a temporary
postoperative Horner’s syndrome in most cases [63–65,67,68,70–72,74,76,
83]. Temporary or permanent vestibular signs (eg, head tilt, nystagmus,
ataxia) have also been reported with that procedure, whereas transient facial
nerve paralysis has only been infrequently encountered [63–65,67,68,70–
72,74,76,83].
The prognosis is excellent with complete removal of the polyp. The
approximate recurrence rate when simple traction is used alone is 30%,
whereas it is less than 8% when accompanied by bulla osteotomy [62,67,75].
Some investigators suggest that corticosteroid administration after simple
traction may aid in further diminishing the risk of a recurrence and that
nasopharyngeal polyps are less likely to recur than aural ones [62].

Canine inflammatory polyps

Not as commonly observed as in the feline species, canine inflammatory
polyps have nonetheless been sporadically described in the literature
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 503

through a few case reports and case series [56,84–86]. The description of the
condition is analogous to the one found for cats, with inflammatory polyps
originating either from the middle ear or Eustachian tube and causing
mostly upper respiratory or middle or external ear disease signs [56,84–86].
Diagnosis is obtained similar to that in the cat (Fig. 5). Likewise, it appears
to be curable with simple traction avulsion or excision through a ventral
bulla osteotomy, with or without total ear canal ablation, when the middle
ear is the site of origin [56,84–86].

Middle ear tumors of the dog and cat

Although nasopharyngeal polyps are well-recognized inflammatory
pathologic lesions affecting predominantly young cats, reports of neoplasia
involving middle ear structures are scarce and poorly described. In a study
of 19 cats treated with tympanic bulla osteotomies for varied middle ear
conditions, 11 ears had surgery for otitis media, 7 for inflammatory polyps,
and 4 for middle ear neoplasia [74]. Of the four cats with malignancies in the
tympanic bulla, three had carcinomas and the fourth had a lymphoblastic
lymphoma. An additional case of feline lymphoma involving the middle ear
was briefly described in a textbook [87]. Although neither of the existing two
reports of feline lymphoma involving the tympanic bulla characterized the
immunophenotype of the malignant lymphocyte population, a case of T-cell

Fig. 5. Video-otoscopic view of a canine inflammatory polyp in the external ear canal of
a Cocker Spaniel. (Courtesy of J.C. Angus, DVM, Urbana, IL.)
504 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509

lymphoma of the tympanic bulla was recently described in an FeLV-

negative cat [88]. Multiple other case reports describe cats with carcinomas
of the middle ear (including 7 cats with SCC), and one reported a fibro-
sarcoma [87,89–95].
Primary neoplasia of the tympanic bulla is equally rare in the dog, with
most reports discussing invasion of the bulla through the tympanic
membrane by predominantly epithelial tumors arising from the external
ear canal [56,96–99]. A study of 11 dogs diagnosed with middle ear tumors
reported one papilloma, two basal cell tumors, three adenocarcinomas of
the ceruminous glands, two papillary adenomas, two sebaceous adenocar-
cinomas, and an anaplastic neoplasia [98]. A case of adenoma originating
from the lining of the Eustachian tube has been reported in a dog, whereas
a malignant jugulotympanic paraganglioma, a tumor of the paraganglion
system, was described as originating from the middle ear in another dog
[100,101]. Another case report documented a fibromyxoma originating from
the middle ear in a geriatric female Boxer [102].
Cholesteatomas are defined as benign masses composed of a matrix of
keratinizing stratified squamous epithelium, inflammatory cells, and keratin
debris [103,104]. They are found only in the middle ear and can be
congenital or acquired. The latter form can be primary or secondary.
Primary acquired cholesteatomas result from chronic otitis media, whereas
secondary acquired cholesteatomas arise after implantation or ingrowth
through a perforation of the tympanic membrane of keratinizing stratified
squamous epithelium into the middle ear. Only acquired cholesteatomas
have been described in the dog [103,104].
The historical presentation of middle ear tumors is often chronic,
mimicking clinical signs of therapy-resistant otitis. The clinical signs of
patients with middle ear tumors are related to the vestibular system (eg,
ataxia, head tilt, loss of balance), to otitis media/externa (eg, head shaking,
otorrhea, pain on opening the mouth, facial nerve paralysis), or to
involvement of the nasopharynx (eg, gagging, upper respiratory dyspnea,
stertor) [56,74,89–95,97–100,102–104]. Diagnosis is obtained with a combi-
nation of signalment, history and clinical signs, visual observation of a mass
via otoscopic examination through an irregular or ruptured tympanic
membrane, high-quality skull radiographs, advanced sectional imaging (CT,
MRI), and histopathology [56,74,82,89,91,92,97–100,103,104]. Imaging of
ear disease has recently been reviewed, and it is well recognized that
advanced sectional imaging, such as CT or MRI, is superior to conventional
radiography, with improved detail and sensitivity, for lesions occurring in
this area of complex architecture [82]. Tissue for biopsy can be obtained
through a myringotomy or via a tympanic bulla osteotomy, often ac-
companied by ear canal ablation.
Therapy for primary middle ear tumors, although infrequently described,
would include tympanic bulla osteotomy, with or without total ear canal
ablation, and surgical removal of the neoplastic tissue through curettage
 T.M. Fan, L-P. de Lorimier / Vet Clin Small Anim 34 (2004) 489–509 505

[56,74,76,96–99]. External beam megavoltage radiation therapy has not been

reported after incomplete surgical excision but would be a logical approach
in such a situation, because the main challenge with tumors of the tympanic
cavity seems to be locoregional control. With lymphoma of the middle ear,
megavoltage radiation therapy could be used without surgery because of the
exquisite radioresponsiveness of that tumor type, and it could be combined
with systemic chemotherapy, because lymphoma tends to be a systemic
disease; however, no reports of treated cases have been published.
Because the incidence of primary middle ear tumors is low, prognosis
after therapy remains to be clearly defined. In a report of 11 dogs with
middle ear tumors, 5 had surgical resection attempted, with survival time
varying between 8 months and 4 years after surgery [98]. In that study, 4 of
the 5 dogs undergoing surgery had benign tumors. Most of the other reports
of malignant middle ear tumors treated with surgery alone tend to speak for
a guarded to poor prognosis [74,76,91,93,95]. A benign lesion, cholestea-
toma can be cured with surgical resection through tympanic bulla
osteotomy accompanied by appropriate medical therapy to control the
chronic otitis media [103].

Summary
Although aural neoplasia is a relatively uncommon entity in companion
animals, it remains a group of heterogeneous conditions that can have
a significant negative impact on quality and duration of life of dogs and cats.
Chronic ear disease that responds poorly or partially to empiric therapy
should raise the suspicion that an underlying condition, such as neoplasia,
may be the perpetrator of inflammation. Early diagnosis followed by ap-
propriate therapy improves the likelihood of disease control and pro-
longed survival.

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