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Figure 15.6. Mechanism of intermittent low pressure pulse therapy. Pressure waves pass through ventilation tube (1) to round window membrane (2) and transmitted to perilymph (yellow) and compress endolymphatic labyrinth (blue) to redistribute endolymph pressure to sac (3) and
blood vessels (4).
SECTION I — Diseases of Ear
through the perilymph and cause reduction in endolymph pressure by redistributing it through various communication channels such as the endolymphatic sac or
the blood vessels (Figure 15.6). Some believe they regulate
secretion of endolymph by the stria vascularis.
Patient can self-administer the treatment at home.
It may require a few months before complete remission
of disease is obtained. Meniett device therapy has been
recommended for patients who have failed medical treatment and the surgical options are being considered.
Chapter 16
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Tumours of External Ear
Of all the cases of ear carcinoma, 85% occur on the pinna,
10% in the external canal and 5% in the middle ear.
Tumours of the external ear may arise from the pinna
or external auditory canal (Table 16.1).
TUMOURS OF AURICLE
BENIGN TUMOURS
1. preauricular sinus or cyst. This results from faulty
union of hillocks of the first and second branchial arches during the development of pinna. Preauricular sinus
presents as a small opening in front of the crus of helix.
It has a branching tract lined by squamous epithelium
which when blocked results in a retention cyst. Patient
usually presents with a cyst which is infected. Surgery is
indicated if there is unsightly swelling or infection. Cyst
or sinus tract must be excised completely to avoid recurrence.
2. sebaceous cyst. Common site is postauricular sulcus
or below and behind the ear lobule. Treatment is total
surgical excision.
3. dermoid cyst. Usually presents as a rounded mass
over the upper part of mastoid behind the pinna.
5. haemangiomas. They are congenital tumours often
seen in childhood. Other parts of face and neck may also
be involved. They are of two types:
(a) Capillary haemangioma. It is a mass of capillary-sized
blood vessels and may present as a “port-wine stain.”
It does not regress spontaneously.
(b) Cavernous haemangioma (also called strawberry tu-
mour). It consists of endothelial-lined spaces filled
with blood. It increases rapidly during the first year
but regresses thereafter and may completely disappear by the fifth year.
(c) Vascular malformation. See Figure 16.2A–C.
6. papilloma (wart). It may present as a tufted growth
or flat grey plaque and is rough to feel. It is viral in origin.
Treatment is surgical excision or curettage with cauterization of its base.
7. cutaneous horn. It is a form of papilloma with
heaping up of keratin and presents as horn-shaped tumour. It is often seen at the rim of helix in elderly people.
Treatment is surgical excision.
8. keratoacanthoma. It is a benign tumour clinically
resembling a malignant one. It presents as a raised nodule
with a central crater. Initially, it grows rapidly but slowly
regresses leaving a scar. Treatment is excision biopsy.
4. keloid. It often follows trauma such as piercing the ear
lobule for ornaments or a surgical incision ( Figure 16.1).
There is a genetic susceptibility. Black races are more often affected. Keloid presents as a pedunculated tumour.
Treatment is surgical excision with injection of triamcinolone into the surgical site or immediate postoperative
radiation of 300 rads.
TABLE 16.1 TUMOURS OF EXTERNAL EAR
Pinna External ear canal
• Benign
• Preauricular cyst or sinus
• Sebaceous cyst
• Dermoid cyst
• Keloid
• Haemangioma
• Papilloma
• Cutaneous horn
• Keratoacanthoma
• Neurofibroma
• Malignant
• Squamous cell carcinoma
• Basal cell carcinoma
• Melanoma
• Benign
• Osteoma
• Exostosis
• Ceruminoma
• Sebaceous adenoma
• Papilloma
• Malignant
• Squamous cell carcinoma
• Basal cell carcinoma
• Adenocarcinoma
• Malignant ceruminoma
• Melanoma
Figure 16.1. Keloid following piercing of an ear lobule for an earring.
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SECTION I — Diseases of Ear
Figure 16.2. Venolymphatic malformation of the pinna in a child (A) patient, (B) during operation and (C) the excised specimen.
often with en bloc removal of parotid gland and cervical
lymph nodes.
2. basal cell carcinoma. The common sites are the
helix and the tragus. It is more common in men beyond
50 years of age. It presents as a nodule with central crust,
removal of which results in bleeding. Ulcer has a raised or
beaded edge. Lesion often extends circumferentially into
the skin but may penetrate deeper, involving cartilage or
bone. Lymph node metastases usually do not occur.
Treatment. Superficial lesions, not involving cartilage,
can be irradiated and cosmetic deformity avoided. Lesions involving cartilage may require surgical excision as
in cases of squamous cell carcinoma.
Figure 16.3. Squamous cell carcinoma of pinna.
9. neuroFibroma. It presents as a nontender, firm swelling and may be associated with von Recklinghausen disease. Treatment is surgical excision, if tumour occludes
ear canal or presents a cosmetic problem.
MALIGNANT TUMOURS
1. squamous cell carcinoma. The site of predilection
is the helix (Figure 16.3). It may present as a painless nodule or an ulcer with raised everted edges and indurated
base. Metastases to regional lymph nodes occur very late.
Disease is more common in males in their fifties who had
prolonged exposure to direct sunlight. Fair-complexioned
people are more prone.
Treatment. Small lesions with no nodal metastases
are excised locally with 1 cm of healthy area around
it. Larger lesions of the pinna or those coming within
1 cm of external auditory canal and lesions with nodal
metastases may require total amputation of the pinna,
3. melanoma. It may occur anywhere over the auricle. It
is more common in men of light complexion who are exposed to sun. Metastases are seen in 16–50% of the cases.
Treatment. Superficial melanoma, less than 1 cm in diameter, situated over the helix, is managed by wedge resection and primary closure.
Superficial melanoma, larger than 1 cm, infiltrative
melanomas, melanoma of posterior auricular surface or
concha and all recurrent melanomas are treated by resection of pinna, parotidectomy and radical neck dissection.
TUMOURS OF EXTERNAL AUDITORY
CANAL
BENIGN TUMOURS
1. osteoma. It arises from cancellous bone and presents
as a single, smooth, bony, hard, pedunculated tumour,
often arising from the posterior wall of the osseous meatus, near its outer end (Figure 16.4). Treatment is surgical
removal by fracturing through its pedicle or removal with
a drill.
2. exostoses. They are multiple and bilateral, often presenting as smooth, sessile, bony swellings in the deeper
part of the meatus near the tympanic membrane. They
Figure 16.4. An osteoma arising from the anterior wall of right
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external auditory canal.
arise from compact bone. Exostosis is often seen in persons exposed to entry of cold water in the meatus as in
divers and swimmers. Males are affected three times more
than females.
Treatment. When small and asymptomatic, no treatment is necessary. Larger ones, which impair hearing or
cause retention of wax and debris, may be removed with
high speed drill to restore normal sized meatus. Exostoses
may extend deeply and lie in close relation to the facial
nerve. Therefore, use of gouge and hammer should be
avoided.
3. ceruminoma. It is a tumour of modified sweat glands
which secrete cerumen. It presents as a smooth, firm,
skin-covered polypoid swelling in outer part of the meatus, generally attached to the posterior or inferior wall. It
obstructs the meatus leading to retention of wax and debris. Malignant type outnumbers the benign by 2:1 ratio.
Treatment. Tumour has a tendency to recur, therefore wide surgical excision should be done and patient
Chapter 16 — Tumours of External Ear
regularly followed up. Some of the ceruminomas are malignant and if there is any suspicion of malignancy on
histology, postoperative radiotherapy should be given.
4. sebaceous adenoma. It arises from sebaceous glands
of the meatus and presents as a smooth, skin-covered
swelling in the outer meatus. Treatment is surgical excision.
5. papilloma. Similar to the one seen on the pinna.
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MALIGNANT TUMOURS
1. squamous cell carcinoma. Most often, it is seen in
cases of long-standing ear discharge. It may arise primarily from the meatus or be a secondary extension from the
middle ear carcinoma.
Presenting symptoms are blood staining of hitherto
mucopurulent or purulent discharge and severe earache.
Examination may show an ulcerated area in the meatus or a bleeding polypoid mass or granulations. Facial
nerve may be paralyzed because of local extension of disease through posterior meatal wall or its spread into the
middle ear. Regional lymph nodes (preauricular, postauricular, infra-auricular and upper deep cervical) may be
involved.
Treatment is en bloc wide surgical excision with postoperative radiation.
2. basal cell and adenocarcinomas. They can rarely
arise from the meatus. Clinical picture is similar to that of
squamous cell variety. Diagnosis is made only on biopsy.
Treatment is wide surgical excision and postoperative radiation.
3. malignant ceruminoma. Malignant type is twice as
common as benign.
4. malignant melanoma. Rare tumour.
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Chapter 17
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Tumours of Middle Ear and Mastoid
CLASSIFICATION
Tumours of middle ear and mastoid can be divided into:
1. Primary tumours
(a) Benign: Glomus tumour
(b) Malignant: Carcinoma, sarcoma
2. Secondary tumours
(a) From adjacent areas, e.g. nasopharynx, external mea-
tus and the parotid.
(b) Metastatic, e.g. from carcinoma of bronchus, breast,
kidney, thyroid, prostate and gastrointestinal tract.
GLOMUS TUMOUR
It is the most common benign neoplasm of middle ear
and is so-named because of its origin from the glomus
bodies. The latter resemble carotid body in structure and
are found in the dome of jugular bulb or on the promontory along the course of tympanic branch of IXth cranial
nerve (Jacobson’s nerve). The tumour consists of paraganglionic cells derived from the neural crest.
AETIOLOGY AND PATHOLOGY
The tumour is often seen in the middle age (40–50 years).
Females are affected five times more.
It is a benign, nonencapsulated but extremely vascular neoplasm. Its rate of growth is very slow and several
years may pass before there is any change from the initial
symptoms. Tumour is locally invasive.
Microscopically, it shows masses or sheets of epithelial
cells which have large nuclei and a granular cytoplasm.
There is abundance of thin-walled blood sinusoids with
no contractile muscle coat, accounting for profuse bleeding from the tumours.
For purposes of diagnosis and treatment, two types are
differentiated.
1. glomus jugulare. They arise from the dome of jugular bulb, invade the hypotympanum and jugular foramen, causing neurological signs of IXth to XIIth cranial
nerve involvement. They may compress jugular vein or
invade its lumen.
2. glomus tympanicum. They arise from the promontory of the middle ear and cause aural symptoms, sometimes with facial paralysis.
Spread of Glomus Tumour
1. Tumour may initially fill the middle ear and later perforate through the tympanic membrane to present as a
vascular polyp.
2. It may invade labyrinth, petrous pyramid and the
mastoid.
3. It may invade jugular foramen and the base of skull,
causing IXth to XIIth cranial nerve palsies.
4. By spread through eustachian tube, it may present in
the nasopharynx.
5. It may spread intracranially to the posterior and middle cranial fossae.
6. Metastatic spread to lungs and bones is rare, but seen
in 4% of cases. Metastatic lymph node enlargement
can also occur.
CLINICAL FEATURES
In 90% of cases, symptoms pertain to the ear.
1. when tumour is intratympanic. Earliest symp-
toms are hearing loss and tinnitus. Hearing loss is conductive and slowly progressive. Tinnitus is pulsatile and
of swishing character, synchronous with pulse and can be
temporarily stopped by carotid pressure.
Otoscopy shows a red reflex through intact tympanic
membrane. “Rising sun” appearance is seen when tumour
arises from the floor of middle ear. Sometimes, tympanic
membrane appears bluish and may be bulging.
“Pulsation sign” (Brown sign) is positive, i.e. when ear
canal pressure is raised with Siegel’s speculum, tumour
pulsates vigorously and then blanches; reverse happens
with the release of pressure.
2. when tumour presents as a polyp. In addition
to hearing loss and tinnitus, there is history of profuse
bleeding from the ear either spontaneously or on attempts to clean it.
Dizziness or vertigo and facial paralysis may appear.
Earache is less common than in carcinoma of the external
and middle ear, and helps to differentiate them from it.
Otorrhoea may occur due to secondary infection and
the condition may simulate chronic suppurative otitis
media with polyp.
Examination reveals a red, vascular polyp filling the
meatus. It bleeds readily and profusely on manipulation
or at biopsy.
3. cranial nerVe palsies. This is a late feature ap-
pearing several years after aural symptoms. IXth to XIIth
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SECTION I — Diseases of Ear
cranial nerves may be paralyzed. There is dysphagia and
hoarseness with unilateral paralysis of the soft palate,
pharynx (IX, X) and vocal cord (X) with weakness of the
trapezius and sternomastoid muscles (XI) and atrophy of
half of tongue (XII).
Tumour may present as a mass over the mastoid or in
the nasopharynx.
Signs of intracranial involvement may also occur.
4. audible bruit. At all stages, auscultation with stethoscope over the mastoid may reveal systolic bruit.
Some glomus tumours secrete catecholamines and produce symptoms like headache, sweating, palpitation, hypertension and anxiety, and require further investigations.
5. rule oF 10s. Remember that 10% of the tumours are
familial, 10% multicentric (occurring in more than one site)
and up to 10% functional, i.e. they secrete catecholamines.
DIAGNOSIS
In addition to thorough history and physical examination, the patient is checked-up to find out the extent
of tumour, other associated glomus tumours and serum
levels of catecholamines or their breakdown products in
urine (vanillylmandelic acid, metanephrine, etc.). Investigations include:
1. computed tomography (ct) scan head. Using
bone window, 1 mm thin sections are cut. It helps to distinguish glomus tympanicum from the glomus jugulare
tumour by identification of caroticojugular spine which
is eroded in the latter. CT scan also helps to differentiate it from the aberrant carotid artery, high or dehiscent
jugular bulb.
2. mri. It shows soft tissue extent of tumour. Magnetic
resonance angiography and venography further help to
delineate invasion of jugular bulb and vein or compression of the carotid artery.
7. biopsy. Preoperative biopsy of the tumour for diagnosis is never done. Clinical and radiologic features are very
characteristic to make diagnosis. Tumour is very vascular
and bleeds profusely. There is also likelihood of injuring
the high jugular bulb or aberrant internal carotid artery if
diagnosis is mistaken.
TREATMENT
It consists of:
1. Surgical removal.
2. Radiation.
3. Embolization.
4. Combination of the above techniques.
Surgical approaches to glomus tumours
1. transcanal approach. Suited for limited glomus
tympanicum tumour where entire circumference of the
tumour is visible, only tympanotomy will suffice to gain
access to the tumour.
2. hypotympanic approach. Suited for tumours limited to promontory with extension to hypotympanum but
not into the mastoid. A superiorly based tympanomeatal
flap is raised by postauricular approach. Bony inferior
tympanic ring is drilled away to see the lower limit of
tumour.
3. extended Facial recess approach. Used for glomus tympanicum extending into mastoid but not into
the jugular bulb. If extensive, modified radical operation
is done.
4. mastoid-neck approach. Used for glomus jugulare
tumours not extending to internal carotid artery, posterior cranial fossa or neck.
5. inFratemporal Fossa approach oF Fisch. Used for
large glomus jugulare tumours.
3. ct head and mri combined. together provide an
excellent preoperative guidance in the differential diagnosis of petrous apex lesions.
4. Four-Vessel angiography. It is necessary when CT
head shows involvement of jugular bulb, carotid artery or
intradural extension. It also helps to delineate any other
glomus tumour (as they may be multiple), find the feeding vessels or embolization of tumour if required.
5. brain perFusion and Flow studies. They are necessary when tumour is pressing on internal carotid artery.
If the case needs surgery, brain perfusion and adequacy of
contralateral internal carotid artery and circle of Willis can
be assessed. If needed, xenon blood flow and isotope studies are done for precise blood flow, and the risk of stroke
and need for surgical replacement of internal carotid artery.
6. emboliZation. In large tumours, embolization of
feeding vessels 1–2 days before operation helps to reduce
blood loss.
6. transcondylar approach. Used for tumours
extending towards foramen magnum. Usually they are
recurrent glomus jugulare tumours. It gives approach to
craniocervical junction with exposure of occipital condyle and jugular tubercle.
Radiation treatment does not cure the tumour but
may reduce its vascularity and arrest its growth. Radiation is used for inoperable tumours, residual tumours,
recurrences after surgery or for older individuals where
extensive skull base surgery is not indicated.
Embolization is used to reduce the vascularity of
tumour before surgery or is the sole treatment in the inoperable patients who have received radiation.
CARCINOMA OF MIDDLE EAR
AND MASTOID
It is a rare condition, there being one case in 20,000 new
patients examined, but it is the commonest primary middle ear malignancy.
AETIOLOGY
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It affects age group of 40–60 years and is slightly more
common in females. Most cases (75%) have associated
long-standing ear discharge. Chronic irritation may be
the causative factor in such cases. Some cases are seen
in radical mastoid cavities. Primary carcinoma of mastoid
air cells is also seen in radium dial painters.
PATHOLOGY
Tumour may arise primarily from middle ear or be an extension of carcinoma of the deep meatus. Squamous cell
variety is by far the most common. Adenocarcinoma may
occasionally be seen; it arises from the glandular elements
of middle ear.
spread oF tumour. To begin with, carcinoma destroys
ossicles, facial canal, internal ear, jugular bulb, carotid canal or deep bony meatus and mastoid. It may spread in petrous pyramid towards its apex. Dura is usually resistant.
It may spread to the parotid gland, temporomandibular
joint, infratemporal fossa and down the eustachian tube
to nasopharynx. Lymph node enlargement occurs late.
Chapter 17 — Tumours of Middle Ear and Mastoid
Figure 17.1. A 4-year-old child with rhabdomyosarcoma of the right
middle ear and mastoid. He also had facial palsy on the same side.
Radiotherapy alone is given as a palliative measure
when tumour involves cranial nerves (IXth to XIIth) or
spreads into the cranial cavity or the nasopharynx.
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CLINICAL FEATURES
Patient often presents with clinical picture simulating
chronic suppurative otitis media. However, the following
features in age group of 40–60 years may arouse suspicion
of malignancy:
1. Chronic foul-smelling discharge especially when blood
stained.
2. Pain which is usually severe and comes at night.
3. Facial palsy.
4. Friable, haemorrhagic granulations or polyp.
5. Appearance of or increase in hearing loss or vertigo.
DIAGNOSIS
Definitive diagnosis is made only on biopsy. Extent of disease is judged by clinical and radiological examination.
CT scan and angiography are useful in the assessment of
disease.
TREATMENT
A combination of surgery and radiotherapy gives better
results. Surgery consists of radical mastoidectomy, subtotal or total petrosectomy depending on the extent of
tumour.
SARCOMAS
• RhabdomyosaRcoma. It is a rare tumour, mostly affecting children. It arises from the embryonic muscles
tissue or the pluripotential mesenchyme. In early stages,
it mimics chronic suppurative otitis media with ear discharge, polyp or granulations. Facial palsy occurs early
(Figure 17.1). Diagnosis is made only on biopsy. Prognosis
is poor. A combination of radiation and chemotherapy is
the treatment of choice. Surgery is done in selected localized lesions.
• otheR saRcomas. Osteosarcoma, lymphoma, fibrosarcoma and chondrosarcoma are rare. Distant metastases
are seen in the lungs or bone. Prognosis is poor.
SECONDARY TUMOURS
Tumours of external auditory meatus, parotid gland or
nasopharynx may invade middle ear cleft either through
the preformed pathways or bone erosion.
Sometimes, temporal bone is the site of distant metastases in advanced cases of carcinoma of the breast,
bronchus, prostate, kidney or gastrointestinal tract.
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Chapter 18
age and sex.
cochleoVestibular symptoms.
cranial nerVe inVolVement
brainstem inVolVement.
cerebellar inVolVement.
raised intracranial tension.
audiological tests.
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Acoustic Neuroma
Acoustic neuroma is also known as vestibular schwannoma, neurilemmoma or eighth nerve tumour.
INCIDENCE
Acoustic neuroma constitutes 80% of all cerebellopontine
angle tumours and 10% of all the brain tumours.
PATHOLOGY
It is a benign, encapsulated, extremely slow-growing tumour of the VIIIth nerve. Microscopically, it consists of
elongated spindle cells with rod-shaped nuclei lying in
rows or palisades. Bilateral tumours are seen in patients
with neurofibromatosis.
ORIGIN AND GROWTH OF TUMOUR
The tumour almost always arises from the Schwann cells of
the vestibular, but rarely from the cochlear division of VIIIth
nerve within the internal auditory canal (Figure 18.1). As it
expands, it causes widening and erosion of the canal and
then appears in the cerebellopontine angle. Here, it may
grow anterosuperiorly to involve Vth nerve or inferiorly
to involve the IXth, Xth and XIth cranial nerves. In later
stages, it causes displacement of brainstem, pressure on
cerebellum and raised intracranial tension (Figure 18.2).
The growth of the tumour is extremely slow and the history may extend over several years.
CLASSIFICATION
Depending on the size, the tumour is classified as:
1. Intracanalicular (when it is confined to internal auditory canal)
2. Small size (up to 1.5 cm)
3. Medium size (1.5–4 cm)
4. Large size (over 4 cm)
Progressive unilateral sensorineural hearing loss, often
accompanied by tinnitus, is the presenting symptom in majority of cases. There is marked difficulty in understanding
speech, out of proportion to the pure tone hearing loss.
This feature is characteristic of acoustic neuroma. Some
patients may get sudden hearing loss.
Vestibular symptoms are imbalance or unsteadiness.
True vertigo is seldom seen.
3.
• Vth nerve. This is the earliest nerve to be involved.
There is reduced corneal sensitivity, numbness or paraesthesia of face. Involvement of this nerve indicates
that the tumour is roughly 2.5 cm in diameter and
occupies the cerebellopontine angle.
• VIIth nerve. Sensory fibres are affected early. There is
hypoaesthesia of posterior meatal wall (Hitzelberger’s
sign), loss of taste (as tested by electrogustometry) and
reduced lacrimation on Schirmer test. Motor fibres are
more resistant and are affected late. Delayed blink reflex may be an early manifestation.
• IXth and Xth nerves. There is dysphagia and hoarseness
due to palatal, pharyngeal and laryngeal paralysis.
• Other cranial nerves. XIth and XIIth, IIIrd, IVth and
VIth are affected when tumour is very large.
4.
ness and numbness of the arms and legs with exaggerated tendon reflexes. They are seen when long motor and
sensory tracts are involved.
5.
cerebellum are seen in large tumours. This is revealed
by finger-nose test, knee-heel test, dysdiadochokinesia,
ataxic gait and inability to walk along a straight line with
tendency to fall to the affected side.
6.
feature. There is headache, nausea, vomiting, diplopia
due to VIth nerve involvement and papilloedema with
blurring of vision.
There is ataxia, weak-
Pressure symptoms on
This is also a late
CLINICAL FEATURES
1.
40–60 years. Both sexes are equally affected.
2.
est symptoms when tumour is still intracanalicular and
are caused by pressure on cochlear or vestibular nerve fibres or on the internal auditory artery.
Tumour is mostly seen in age group of
They are the earli-
INVESTIGATIONS AND DIAGNOSIS
Attempts should be made to diagnose the tumour in its
otological phase when it is still intracanalicular. This
is possible when all cases of unilateral sensorineural
hearing loss with tinnitus or imbalance are carefully
evaluated.
1.
tween cochlear and retrocochlear lesions.
See Table 15.1 for difference be-
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