Anatomy of the EAR

The ear consists of the external ear, the middle ear, and the inner ear. The
external ear includes the auricle, external auditory meatus, and the tympanic
membrane (ear drum). The middle ear is a cavity in which the ossicles or small
bones of the ear are suspended. The inner ear encloses organs of hearing and
balance.

External ear

 The auricle is the visible external appendage of the ear. It is

composed of yellow elastic cartilage covered by thin skin.
 The external auditory meatus extends from the auricle to
the tympanic membrane. The external 1/3 is composed of
elastic cartilage and the internal 2/3 is bony. The skin that
lines the meatus has hairs, sebaceous glands, and
ceruminous glands, which secrete the earwax, cerumen. This
waxy substance keeps the skin moist and traps insects.

Middle ear

 The middle ear is a cavity (the tympanic cavity), which communicates

with the pharynx by the auditory tube and with the mastoid air cells in
the mastoid process of the temporal bone.
 The cavity and its contents are lined mostly by squamous or low
cuboidal epithelium.
 Three small ossicles (malleus, incus, and stapes) traverse the tympanic
cavity.
 The malleus is attached to the tympanic membrane;
 The incus connects the malleus and the stapes;
 The stapes is attached to the oval window.
 Two small muscles, the tensor tympani, which inserts on the malleus,
and the stapedius, which inserts on the stapes, dampen the
movements of the ossicles so that high frequency vibrations do not
damage the ear.
 The fenestra ovalis (oval window) separates the tympanic cavity from
the vestibule of the osseous labyrinth
 fenestra rotunda separates the tympanic cavity from the scala tympani
of the cochlea.
 The auditory tube is usually closed but opens during swallowing to
equalize air pressure on both sides of the tympanic membrane.

The inner ear

 Consider the inner ear as comprising two systems of canals and cavities.
The osseous (bony) labyrinth is a system of canals and cavities within the
petrous part of the temporal bone. This labyrinth is filled with perilymph. The
membranous labyrinth can be thought of as floating within the osseous
labyrinth. The membranous labyrinth contains endolymph.

The osseous labyrinth

 Medial to the tympanic cavity, the osseous labyrinth is expanded into

the vestibule.
 The fenestra ovalis is in the wall that separates the vestibule from
the tympanic cavity.
 The semicircular canals, which are continuations of the osseous
labyrinth, open into the vestibule.
 Near the opening of each canal into the vestibule is a swelling, the
ampulla.
 There are three semicircular canals arranged at right angles to each
other. They are designated superior, anterior, and inferior.
 The vestibule is also continuous with the bony cochlea. The
cochlea is a spirally coiled tube that makes 2 and 3/4 turns. Its
center support is the bony modiolus.
 The spiral lamina is a bony shelf that projects from the modiolus.

 Medial to the tympanic cavity, the osseous labyrinth is expanded into

the vestibule.
 The fenestra ovalis is in the wall that separates the vestibule from
the tympanic cavity.
 The semicircular canals, which are continuations of the osseous
labyrinth, open into the vestibule.
 Near the opening of each canal into the vestibule is a swelling, the
ampulla.
 There are three semicircular canals arranged at right angles to each
other. They are designated superior, anterior, and inferior.
 The vestibule is also continuous with the bony cochlea. The
cochlea is a spirally coiled tube that makes 2 and 3/4 turns. Its
center support is the bony modiolus.
 The spiral lamina is a bony shelf that projects from the modiolus.

The membranous labyrinth is in some places adherent to the

osseous labyrinth but in most places is separated from it by the
perilymph.
The utricle and saccule are two dilatations of the membranous
labyrinth in the vestibule.
The utricle is a connecting chamber that communicates with the
semicircular canals.
The saccule communicates with the utricle and the two combine to
form the endolymphatic duct, a sac that ends blindly in the temporal
bone. The saccule also communicates with the cochlear duct.
 ASSESSMENT
Inspection of External Ear

Inspect for deformities, lesions and discharge, symmetry and angle of

attachment.

Otoscopic Exam

Used to examine external auditory canal and tympanic membrane

Procedure:
1 .Otoscope is held at the right hand of the examiner
2. It should be in pencil position
3. Left hand hold the pinna back to straighten the canal

Evaluation of Gross Auditory Acuity

A. Whisper Test
Exclude one ear from testing, then examiner whisper softly from distance of
1 or 2 ft. from the patient.
The person with normal hearing acuity can correctly repeat what was
whispered.

B. Weber's Test
Use tuning fork (512 Hz)
Use bone conduction to test lateralization of sound
tapping of tuning fork and placed on patient head or forehead

The result is:

 Normal tone heard in the center of the head or equally in both
ears
 Conductive Hearing Loss heard better on affected ear
 Sensorineural Hearing Loss heard on better hearing ear

C. Rinne's Test
 Compares air conduction from bone conduction; differentiates conductive
and sensorineural
hearing loss
 The vibrating tuning fork is placed against the mastoid bone; then, it is
placed 2 inches from the opening of the ear canal
 Normal: air conduction is better than bone conduction
 DIAGNOSTIC PROCEDURES

AUDIOMETRY
 The single most important diagnostic instrument in detecting hearing
loss.
 Patient wears earphones and signal to audiologist if tone is heard.

TYPES:
 Pure-Tone Audiometry - uses musical tone
- The louder the tone perceived by the patient, the
greater the hearing loss.

 Speech Audiometry - Spoken words is used to determine ability to

hear and discriminate sounds and words
- The louder the sound perceived by the patient,
the greater the hearing loss.

TYMPANOGRAM
 also known as Impedance Audiometry
 measures middle ear muscle reflex to sound stimulation and compliance
of tympanic membrane by changing the air pressure in sealed ear
canal.

AUDITORY BRAIN STEM RESPONSE

 Detectable electrical potential from CNVIII and the ascending auditory
pathways of brainstem in response to sound stimulation.
 Electrodes placed on the patients forehead
 The electrode physiologic measurement can determine at which decibel
level a patient hears.

MIDDLE EAR ENDOSCOPY

 use of very small diameter endoscopes
 done as an office procedure to evaluate suspected perilymphatic fistula

How it is done?

 Tympanic membrane is anesthetized topically for 10 minutes

 External Auditory canal is irrigated with NSS
 With aid of microscope a tympanotomy is created with laser
beam or myringotomy knife so that endoscope can be inserted in
middle ear.
 .

HEARING LOSS

To understand hearing loss it is important to understand how normal hearing takes

place. There are 2 different pathways by which sound waves produce the
sensation of hearing: air conduction and bone conduction.

• In air conduction, sound waves move through the air in the external
auditory canal (the "ear canal" between the outside air and your eardrum).
The sound waves hit the tympanic membrane (eardrum) and cause the
tympanic membrane to move.

• The bones in the middle ear are connected to the tympanic membrane.
When the tympanic membrane moves, this movement is transmitted to the
bones. These 3 bones are called the malleus, the incus, and the stapes.
Movement of the stapes causes pressure waves in the fluid-filled inner ear.

• The cochlea is an inner ear structure surrounded by fluid. It contains

multiple small hairs. Pressure waves in the fluid cause the hairs to move.
This movement stimulates the auditory nerve. Different frequencies of
noises stimulate different hairs on the cochlea, which translate to the
sensation of sounds of different pitch.

• Hearing by bone conduction occurs when a sound wave or other source of

vibration causes the bones of the skull to vibrate. These vibrations are
transmitted to the fluid surrounding the cochlea and hearing results.

Conductive hearing loss

 usually results from external ear disorder, such as impacted
cerumen, or a middle ear disorder, such as otitis mediator
otosclerosis
 efficient transmission of sound by air to the inner ear is
interrupted
 a sensor neural loss involves damage to the cochlea or
vestibularcochlear nerve
 disorder often can be corrected with no damage to hearing or
minimal permanent hearing loss
 Causes:
 obstruction of the external or middle ear
 tumors
 otosclerosis
 a buildup of scar tissue on the ossicles
 previous middle ear surgery

Sensorineural hearing loss

 Is a pathological process of the inner ear or of the sensory fibers that

lead to cerebral cortex
 is often permanent, and measures must be taken to reduce further
damage or to attempt to amplify sound as a means of improving hearing
to some degree

Causes
 damaged to the inner ear structure
 damaged to the 8th cranial nerve
 prolonged exposure to loud noise
 medications
 trauma
 inherited disorders
 metabolic and circulatory disorders
 infections
 surgery
 Meniere’s syndrome
 Diabetes mellitus
 Myxedema

Mixed hearing loss

has conductive loss and sensorineural loss, resulting from
dysfunction of air and bone conduction.

Clinical manifestation

 tinnitus
 increasing inability to hear in groups
 need to turn up the volume of television or radio
 frequently asking to repeat the statements
 turning head or leaning forward to favor one ear
 shouting in conversation
 ringing the ears
 failing to respond when not looking in the direction of the sound
 answering the questions incorrectly
 withdrawing from social interactions

Medical management
Aural Rehabilitation

Nursing management
 trying to speak in a loud voice to a person who cannot hear
high frequency sounds only makes understanding more
difficult
 during health care and screening procedures, the practitioner
must be aware that patients who are deaf or hearing
impaired are unable to red lips, see a signer, or read written
materials in dark room required during some diagnostic test

Conditions of the inner ear

  Disorders of balance and the vestibular system involving system involving
the inner ear
 The term dizziness is used frequently by patient and health care provides
to describe any altered sensation of orientation in space.
 Vertigo is defined as the misperception or illusion of motion of the person
or the surroundings.
 Ataxia is a failure of muscular coordination and may be present in patient
with vestibular disease.
 Syncope, fainting, and loss of consciousness are not forms of vertigo nor
ease in they characteristic of an ear problem they usually indicate disease
in the cardiovascular system.
 Nystagmus is an involuntary rhythmic movement of the eyes.

Motion sickness

 Motion sickness is a normal response to real, perceived, or anticipated

movement.
 People tend to experience motion sickness on a moving boat, train,
airplane, automobile, or amusement park rides.
 Although this condition is common and only a minor nuisance for the
occasional traveler, it may be incapacitating for people with an occupation
that requires constant movement, such as a flight attendant, pilot,
astronaut, or ship crewmember.
 Symptoms generally consist of dizziness, fatigue, and nausea, which may
progress to vomiting.
 Fortunately, most symptoms disappear once the journey is over.

Signs and Symptoms

The most common signs and symptoms of motion sickness include:

• Nausea
• Paleness of the skin
• Cold sweats
• Vomiting
• Dizziness
• Headache
• Increased salivation
• Fatigue
Causes

Motion sickness occurs when the body, the inner ear, and the eyes send
conflicting signals to the brain.
This reaction is generally provoked by a moving vehicle such as a car,
boat, airplane, or space shuttle, but it may also happen on flight simulators
or amusement park rides.
From inside a ship's cabin, the inner ear may sense rolling motions that
the eyes cannot perceive, and, conversely, the eyes may perceive
movement on a "virtual reality" simulation ride that the body does not feel.
Interestingly, once a person adapts to the movement and the motion stops,
the symptoms may recur and cause the person to adjust all over again
(although, this reaction is generally brief).
In addition, even anticipating movement can cause anxiety and symptoms
of motion sickness.

Risk Factors

The following are the most common risk factors for motion sickness:

• Riding in a car, boat, airplane, or space shuttle

• Age -- children between the ages of 2 - 12 are most at risk. Occurrence of
motion sickness declines with age (this is probably due to behavioral
changes and coping strategies rather than anything inherent in the aging
process).
• Susceptibility to nausea or vomiting
• Heightened level of fear or anxiety
• Exposure to unpleasant odors
• Poor ventilation
• Spending long hours at a computer screen
• Being outside of the earth's gravitational force

Diagnosis

Most people who have experienced motion sickness in the past ask their
health care provider how to prevent another episode from occurring in the
future.
Rarely will an individual arrive at his or her health care provider's office
actually experiencing motion sickness.
To establish a diagnosis of motion sickness, the provider will inquire about
the individual's symptoms as well as the event that typically causes the
condition (such as riding in a boat, flying in a plane, or driving in car).
Laboratory tests are generally not necessary to establish a diagnosis of
motion sickness.
Preventive Care

The following general measures may be taken to help avoid the discomfort
caused by motion sickness:

• Reduce anxiety and fears, particularly through methods such as cognitive-

behavioral therapy and biofeedback.
• Use head rests to minimize head movements.
• Maintain proper ventilation to decrease foul odors that may cause nausea.
• Stay occupied to distract the mind from thinking about motion sickness.
Reading may worsen symptoms.
• Particular exercises, such as tumbling or jumping on a trampoline, may
desensitize an individual prior to being in a situation that causes motion
sickness.

Individuals who commonly experience motion sickness on a plane should take the
following preventive measures:

• Avoid bulky, greasy meals and overindulgence in alcoholic beverages the

night before air travel.
• Eat light meals or snacks that are low in calories in the 24 hours before air
travel.
• Avoid salty foods and dairy products before air travel.
• Sit toward the front of the aircraft or in a seat by the wing because the ride
will feel smoother in these locations.
• Eat foods high in carbohydrates before air travel.

Individuals with a tendency toward motion sickness on a boat should take the
following preventive measures:

• Passengers below the deck should keep their eyes closed and minds
occupied (by engaging in conversation, for example).
• Passengers on the deck should keep their eyes fixed on the horizon or
visible land.
Treatment

 While medications may be an acceptable treatment for travelers who

occasionally experience motion sickness,
 The goal for individuals who experience motion sickness on a regular basis
or whose work is affected by their symptoms is to learn to control -- and
eventually prevent -- these symptoms.
 This may be accomplished with mind-body practices, such as cognitive-
behavioral therapy and biofeedback.
 Other alternatives to medication include homeopathy, acupuncture, dietary
supplements, dietary changes, and physical exercise.

Medications

Medications for motion sickness may cause drowsiness and impair judgment and,
therefore, should be avoided in pilots, astronauts, ship crew members, and
individuals in any other occupation where heavy equipment is operated or where
being alert is critical. The following medications are a reasonable option for
infrequent travelers and others who experience motion sickness occasionally:

• Scopolamine -- most commonly prescribed medication for motion sickness.

It must be taken before the onset of symptoms. It is available in patch form
that is placed behind the ear 6 - 8 hours before travel. The effects last up to
3 days. Side effects may include dry mouth, drowsiness, blurred vision, and
disorientation.
• Promethazine -- take 2 hours before travel. The effects last between 6 - 8
hours. Side effects may include drowsiness and dry mouth.
• Cyclizine -- most effective when taken at least 30 minutes before travel. It is
not recommended for children younger than 6, and side effects are similar
to scopolamine.
• Dimenhydrinate -- take every 4 - 8 hours. Side effects are similar to
scopolamine.
• Meclizine -- most effective when taken 1 hour before travel. It is not
recommended for children under 12, and side effects may include
drowsiness and dry mouth
 Ménière's disease

 Is a disorder of the inner ear that can affect hearing and balance.
 It is characterized by episodes of dizziness and tinnitus and
progressive hearing loss, usually in one ear.
 It is caused by an increase in volume and pressure of the
endolymph of the inner ear.
 It is named after the French physician Prosper Ménière, who first
reported that vertigo was caused by inner ear disorders in an
article published.

Symptoms

The symptoms of Meniere’s are variable; not all sufferers experience the same
symptoms. However, so-called "classic Meniere’s is considered to comprise the
following four symptoms:

• Periodic episodes of rotary vertigo (the abnormal sensation of movement)

or dizziness.
• Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears)
hearing loss, often initially in the lower frequency ranges.
• Unilateral or bilateral tinnitus (the perception of noises, often ringing,
roaring, or whooshing), sometimes variable.
• A sensation of fullness or pressure in one or both ears.

Meniere’s often begins with one symptom, and gradually progresses. A diagnosis
may be made in the absence of all four classic symptoms.

Attacks of vertigo can be severe, incapacitating, and unpredictable. In some

patients, attacks of vertigo can last for hours or days, and may be accompanied
by an increase in the loudness of tinnitus and temporary, albeit significant, hearing
loss in the affected ear(s). Hearing may improve after an attack, but often
becomes progressively worse. Vertigo attacks are sometimes accompanied by
nausea, vomiting, and sweating.

Some sufferers experience what are informally known as "drop attacks" — a

sudden, severe attack of dizziness or vertigo that causes the sufferer, if not
seated, to fall. Patients may also experience the feeling of being pushed or pulled
(Pulsion). Some patients may find it impossible to get up for some time, until the
attack passes or medication takes effect. There is also the risk of injury from
falling.
In addition to hearing loss, sounds can seem tinny or distorted, and patients can
experience unusual sensitivity to noises (hyperacusis). Some sufferers also
experience nystagmus, or uncontrollable rhythmical and jerky eye movements,
usually in the horizontal plane, reflecting the essential role of the balance system
in coordinating eye movements.

Cause

 The exact cause of Meniere’s disease is not known, but it is believed to

be related to endolymphatic hydrops or excess fluid in the inner ear.
 It is thought that endolymphatic fluid bursts from its normal channels in
the ear and flows into other areas causing damage.
 This may be related to swelling of the endolymphatic sac or other
tissues in the vestibular system of the inner ear, which is responsible for
the body's sense of balance.
 The symptoms may occur in the presence of a middle ear infection,
head trauma or an upper respiratory tract infection, or by using aspirin,
smoking cigarettes or drinking alcohol.
 They may be further exacerbated by excessive consumption of caffeine
and salt in some patients.
 Excessive levels of potassium in the body (usually caused by the
consumption of potassium rich foods) may also exacerbate the
symptom

Diagnosis

detailed oto-neurological examination,

audiometry
Head magnetic resonance imaging (MRI) scan should be performed to
exclude a tumour of the cranial nerve VIII (vestibulocochlear nerve) which
would cause similar symptoms.

Treatment

Initial treatment is aimed at both dealing with immediate symptoms and preventing
recurrence of symptoms, and so will vary from patient to patient. Doctors may
recommend vestibular training, methods for dealing with tinnitus, stress reduction,
hearing aids to deal with hearing loss, and medication to alleviate nausea and
symptoms of vertigo.

Several environmental and dietary changes are thought to reduce the frequency
or severity of symptom outbreaks. Most patients are advised to adopt a low-
sodium diet, typically one to two grams (1000-2000mg) at first, but diets as low as
400mg are not uncommon. Patients are advised to avoid caffeine, alcohol and
tobacco, all of which can aggravate symptoms of Ménière's. Some recommend
avoiding Aspartame. Patients are often prescribed a mild diuretic (sometimes
vitamin B6). Many patients will have allergy testing done to see if they are
candidate for allergy desensitization as allergies have been shown to aggravate
Ménière's symptoms.

Women may experience increased symptoms during pregnancy or shortly before

menstruation, probably due to increased fluid retention.

Lipoflavonoid is also recommended for treatment by some doctors.

Many patients consider fluorescent lighting to be a trigger for symptoms. The

plausibility of this can be explained by how important a part vision plays in the
overall mechanism of human balance.

Treatments aimed at lowering the pressure within the inner ear include
antihistamines, anticholinergics, steroids, and diuretics. A medical device that
provides transtympanic micropressure pulses is now showing some promise and
is becoming more widely used as a treatment for Ménière's.

Surgery may be recommended if medical management does not control vertigo.

Injection of steroid medication behind the eardrum, or surgery to decompress the
endolymphatic sac may be used for symptom relief. Permanent surgical
destruction of the balance part of the affected ear can be performed for severe
cases if only one ear is affected. This can be achieved through chemical
labyrinthectomy, in which a drug (such as gentamicin) that "kills" the vestibular
apparatus is injected into the middle ear. The nerve to the balance portion of the
inner ear can be cut (vestibular neurectomy), or the inner ear itself can be
surgically removed (labyrinthectomy). These treatments eliminate vertigo, but
because they are destructive, they are used only as a last resort. Typically
balance returns to normal after these procedures, but hearing loss may continue
to progress.

MEDICATIONS USED BETWEEN ATTACKS

Diuretic -- that in common use all tend to be carbonic anhydrates inhibitors, or
combinations, for reasons that are not entirely clear. These agents have the
advantage that they may not require potassium supplementation.

• Dyazide (triamterine/HCTZ).
• Moduretic(amiloride/HCTZ)
• Diamox (acetazolamide)

Notes: as triamterine is a folate antagonist, pregnant women should take folate

supplements if not otherwise contraindicated. Occasionally persons on long-term
acetazolamide develop kidney stones.

Vestibular Suppressants
 • Clonazepam(Klonapin) 0.5 mg twice a day or as needed
• lorazepam (Ativan) 0.5mg twice a day or as needed
• diazepam (Valium) 2 mg twice a day or as needed
• meclizine (Antivert ) 12.5 mg to 25 mg as needed up to 3-4 times/day

Calcium Channel Blockers

• Verapamil (Calan, Isoptin, Verelan are brand names) 120-240 mg.

Sustained release should be used.
• Nimodipine
• Flunarizine/Cinnarizine (not available in the USA)

Steroids (commonly for severe bouts)

• Dexamethasone
• Prednisone
• Methylprednisoline

Immune suppressants

• Methotrexate
• Steroids (see above)
• Enbrel (injectable drug)

Agents that are controversial

• Serc (betahistine) -- commonly used, may be placebo, but often worth

trying.
• Histamine injections (irrational treatment as Histamine is broken down
rapidly in the body).
• Homeopathic treatments, such as Vertigo Heel. As is the case with all
homeopathic treatments, Vertigo Heel is probably a placebo.
• Antiviral therapy (such as acyclovir, no evidence for effectiveness)
• Intratympanic dexamethasone or other steroids (becoming more common,
little evidence for effectiveness)
Surgery and Destructive Treatments of Meniere's

The main role of surgical treatment is to manage intractable vertigo. Surgical

treatment have not been shown to preserve hearing to any greater extent than
medical treatments

Trans (intra) tympanic injection of Gentamicin for control of intractable Meniere's

disease. This method can also be used to inject steroids

Labyrinthitis

 inflammation of the inner ear structure called the labyrinth.

 refers to other causes of inner ear problems that have no
inflammation because those problems produce similar
symptoms.

• You have a labyrinth in each of your inner ears, encased in thick bone near
the base of your skull. As the name implies, the labyrinth is a maze of
interconnected fluid-filled channels and canals. Half of the labyrinth, the
cochlea, is shaped like a snail’s shell. It sends information about sounds to
the brain. The other half looks something like a gyroscope with 3
 semicircular canals connected to an open cavern or vestibule. The
vestibule portion of the labyrinth sends information to the brain regarding
the position and movement of your head. Any disturbance of the vestibule
can lead to faulty information going to your brain.

• Your eyes also send positioning information to your brain. When

information from the labyrinth and the eyes don’t match, the brain has
trouble interpreting what is happening. This misinterpreting often leads to a
sensation that you are spinning (vertigo) or a feeling that you are moving
when in fact you are remaining still. Feelings of motion sickness (nausea
and vomiting) often follow. Sometimes you will experience hearing loss or
abnormal sounds such as a high- or low-pitched ringing (tinnitus).

Causes

Many times, you cannot determine the cause of labyrinthitis. Often, the condition
follows a viral illness such as a cold or the flu. Viruses, or your body’s immune
response to them, may cause inflammation that results in labyrinthitis.

Other potential causes are these:

• Trauma or injury to your head or ear

• Bacterial infections: If found in nearby structures such as your middle ear,

such infections may cause the following:

o Fluid to collect in the labyrinth (serous labyrinthitis)

o Fluid to directly invade the labyrinth, causing pus-producing

(suppurative) labyrinthitis
• Allergies

• Alcohol abuse

• A benign tumor of the middle ear

• Certain medications taken in high doses

o Furosemide (Lasix)

o Aspirin

o Some IV antibiotics

o Phenytoin (Dilantin) at toxic levels

 • Benign paroxysmal positional vertigo: With this condition, small stones, or
calcified particles, break off within the vestibule and bounce around. The
particles trigger nerve impulses that the brain interprets as movement.

• More serious causes of vertigo can mimic labyrinthitis, but these occur
rarely.

o Tumors at the base of the brain

o Strokes or insufficient blood supply to the brainstem or the nerves

surrounding the labyrinth

Symptoms

• The most common symptoms

o Vertigo

o Nausea

o Vomiting

o Loss of balance

• Other possible symptoms

o A mild headache

o Tinnitus (a ringing or rushing noise)

o Hearing loss

• These symptoms often are provoked or made worse by moving your head,
sitting up, rolling over, or looking upward.

• Symptoms may last for days or even weeks depending on the cause and
severity.

o Symptoms may come back, so be careful about driving, working at

heights, or operating heavy machinery for at least 1 week from the
time the symptoms end.
 o Rarely, the condition may last all your life, as with Ménière disease.
This condition usually involves tinnitus and hearing loss with the
vertigo. In rare cases it can be debilitating.

o Do 6-10 repetitions, 3 times per day.

Treatment

Self-Care at Home

• Lie still in a comfortable position, often flat on your side.

• Reduce your salt and sugar intake.

• Avoid chocolate, coffee, and alcohol.

• Stop smoking.

• Try to create a low-noise, low-stress environment.

• Talk to your doctor about certain maneuvers or exercises (Brandt and

Daroff exercises and Epley maneuver) that may speed your recovery.
These positions attempt to rearrange tiny particles inside your ear and/or
desensitize you to their effects.

o Sit on the edge of your bed near the middle, with legs hanging
down.

o Turn your head 45° to your right side.

o Quickly lie down on your left side, with your head still turned, and
touch the bed with the portion of your head behind your ear.

o Hold this position—and every following position—for about 30

seconds.

o Sit up again.

o Quickly turn your head 45° toward your left side and lie down on
your right side.

o Sit up again.

o Do 6-10 repetitions, 3 times per day.

Medication

Patients with labyrinthitis are given antibiotics, either by mouth or intravenously to

clear up the infection. They may also be given meclizine (Antivert, Bonine) for
vertigo and nausea.

Surgery

Some patients require surgery to drain the inner and middle ear.

Supportive care

Patients with labyrinthitis should rest in bed for three to five days until the
acute dizziness subsides.
Patients who are dehydrated by repeated vomiting may need intravenous fluid
replacement.
Patients are advised to avoid driving or similar activities for four to six weeks
after the acute symptoms subside, because they may have occasional dizzy
spells during that period.

Prognosis

Most patients with labyrinthitis recover completely, although it often takes five to
six weeks for the vertigo to disappear completely and the patient's hearing to
return to normal. In a few cases, the hearing loss is permanent.

Prevention

The most effective preventive strategy includes prompt treatment of middle ear
infections, as well as monitoring of patients with mumps, measles, influenza, or
colds for signs of dizziness or hearing problems.

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Is a brief period of incapaciting vertigo that occur s when the

position of the patient’s head is changed with respect to
gravity, typically by placing the head back with the affected
ear turned down.
due to debris which has collected within a part of the inner
ear. This debris can be thought of as "ear rocks", although
the formal name is "otoconia"
 Causes
head injury in age 50 years and above
association with migraine
is degeneration of the vestibular system of the inner ear
 This is common in older age
vestibular neuritis

Clinical manifestation

 Sudden onset followed by a predisposition for positional vertigo,

usually for hours to week but occasionally for months or years
 Due to the disruption of debris is form from small crystals of calcium
carbonate from the inner ear structure, the utricle
 Stimulated by head trauma
 Infection
 Severe cases of vertigo is usually accompanied by nausea and
vomiting
 Hearing impairment does not generally occur
 dizziness or vertigo
 lightheadedness
 imbalance
 nausea

Nursing management

 Bed rest for patients with acute symptoms

 Canalith repositioning – this is non-invasive procedure, which
involves quick movements of the body, rearranges the debris in the
canal
-this procedure is performed by placing the patient in a sitting
position, turning the head to a 45 degree angle on the affect side,
and then quickly moving the patient to the supine position
- This position is safe, inexpensive, and easy to perform
 Medical management

 Meclizine – drugs for patients with acute vertigo used for 1-2 weeks
 Prochlorperazine – for patient with severe vertigo, 1 hr before the
canalith repositioning procedure is performed
 Vestibular rehabilitation – used in the management of vestibular
disorders
- this strategy promotes active used of the vestibular
system through an interdisciplinary team approach,
including medical therapy.

Condition of the middle ear

SEROUS OTITIS MEDIA

• Serous Otitis Media (middle ear effusion) involves fluid, without evidence of
active infection, in the middle ear.
• This fluid results from a negative pressure in the middle ear caused by
eustachian tube obstruction.
• When this condition occurs in adults, an underlying cause for the
eustachian tube dysfunction must be sought.
• Middle ear effusion is frequently seen in patients after radiation therapy or
barotrauma and in patients with eustachian tube dysfunction from a
concurrent upper respiratory infection or allergy.
• Barotrauma results from sudden pressure changes in the middle ear
caused b changes in barometric pressure, as in scuba diving or airplane
descend.
• A carcinoma obstructing the eustachian tube should be ruled out in adults
with persistent unilateral serous otitis media.

CLINICAL MANIFESTATIONS
• Patients may complain of hearing loss, fullness in the ear or a sensation of
congestion, or popping and crackling noises, which occur as the
eustachian tube attempts to open.
• The tympanic membrane appears dull on otoscopy, and air bubbles may be
visualized in the middle ear.
• Usually, the audiogram shows a conductive hearing loss.

MANAGEMENT
• Serous Otitis Media need to b treated medically unless infection occurs.
• If the hearing loss associated with middle ear effusion is significant, a
myringotomy can be performed and a tube may be placed to keep the
middle ear ventilated.
• Corticosteriods in small doses may decrease the edema of the eustachian
tube in case of barotrauma.
• Decongestant have not been proven effective.
• A valsalva maneuver, which forcibly opens the eustachian tube, may be
cautiously performed; this maneuver may cause worsening pain or
perforation of the tympanic membrane.

ASSESSMENT FINDINGS

PNEUMATIC OTOSCOPY:
• Clinicians should use pneumatic otoscopy as the primary diagnostic
method for OME. OME should be distinguished from AOM. Strong
 Recommendation based on systematic review of cohort studies and
preponderance of benefit over harm.

TYMPANOMETRY:
• Tympanometry can be used to confirm the diagnosis of OME. Option based
on cohort studies and a balance of benefit and harm.

MEDICATION

• Antihistamines and decongestants are ineffective for OME and are not
recommended for treatment.
• Antimicrobials and corticosteroids do not have long-term efficacy and are
not recommended for routine management.
• Although statistically significant benefits have been demonstrated for some
medications, they are short term and relatively small in magnitude.
• The prior OME guideline found no data supporting antihistamine-
decongestant combinations in treating OME.
• Long-term benefits of antimicrobial therapy for OME are unproved despite
a modest short-term benefit for 2 to 8 weeks in randomized trials.
• Adverse effects of antimicrobials are significant and may include rashes,
vomiting, diarrhea, allergic reactions, alteration of the child’s
nasopharyngeal flora, development of bacterial resistance, and cost.
• The prior OME guideline did not recommend oral steroids for treating OME
in children. A later meta-analysis showed no benefit for oral steroid versus
placebo within 2 weeks, but did show a short-term benefit for oral steroid
plus antimicrobial versus antimicrobial alone in 1 out of 3 children treated.
• This benefit became non significant after several weeks in a prior meta-
analysis and in a large randomized trial. Oral steroids can produce
behavioral changes, increased appetite, and weight gain.
• Additional adverse effects may include adrenal suppression, fatal varicella
infection, and avascular necrosis of the femoral head.
• Although intranasal steroids have fewer adverse effects, one randomized
trial showed statistically equivalent outcomes at 12 weeks for intranasal
beclomethasone plus antimicrobials versus antimicrobials alone for OME.
• Antimicrobial therapy, with or without steroids, has not been demonstrated
to be effective in long-term resolution of OME, but in some cases this
therapy can be considered an option because of short-term benefit in
randomized trials, when the parent or caregiver expresses a strong
aversion to impending surgery. In this circumstance a single course of
therapy for 10 to 14 days may be used.
• The likelihood that the OME will resolve long term with these regimens is
small, and prolonged or repetitive courses of antimicrobials or steroids are
strongly not recommended.
 • Other nonsurgical therapies that are discussed in the OME literature
include autoinflation of the eustachian tube, oral or intratympanic use of
mucolytics, and systemic use of pharmacologic agents other than
antimicrobials, steroids and antihistamine-decongestants.

CHRONIC OTITIS MEDIA

• Chronic Otitis media is the result of recurrent AOM causing irreversible tissue
pathology and persistent perforation of the tympanic membrane.
• Chronic infection of the middle ear damage the tympanic membrane, destroy
the ossicles and involve the mastoid.
• Before the discovery of antibiotics, infections of the mastoid were life-
threatening. Today, acute mastoditis is rare in developed countries.

CLINICAL MANIFESTATIONS
• Symptoms may be minimal, with varying degrees of hearing loss and a
persistent or intermittent, foul smelling otorrhea.
• Pain is not usually experienced, expect in cases of acute mastoditis, when the
postauricular area is tender and may be erythematous and edematous.
• Otoscopic examination may show a perforation and cholesteatoma can be
identified as a white mass behind the tympanic membrane or coming through
the external canal from a perforation.
• Cholesteatoma is an ingrowth of the skin of the external layer of the eardrum
into the middle ear.
• It is generally caused by a chronic retraction pocket of the tympanic membrane
creating a high negative pressure of the middle ear.
• The skin forms a sac that feels with degenerated skin and sebaceous
materials.
• The sac can be attached to the structures of the middle ear or mastoid or both.
• Chronic Otitis media can cause chronic mastoiditis and lead to the formation of
cholesteatoma.
• It can occur in the middle ear, mastoid cavity or both, often dictating the type of
surgery to be performed.
• If untreated, cholesteatoma will continue to enlarge, possibly causing damage
to the facial nerve and horizontal canal and destruction of other surrounding
structure.
• Cholesteatomas are the third most common benign tumor of the ear, seen in
approximately 9.2 people per 100,000 people annually.
• Cholesteatomas usually do not cause pain; however, if treatment or surgery is
delayed, they may destroy structures of the temporal bone.
• These fast-growing tumors may cause severe sequelae such as hearing loss
or neurologic disorders.
• Congenital cholesteatomas are usally found in children and may cause severe
bone loss of the incus.
• Cholesteatomas found in elderly patients generally develop in external canal.
• Cholesteatomas may be asymptomatic or they may cause hearing loss, facial
pain and paralysis, tinnitus, or vertigo.
• Audiometric tests often show a conductive or mixed hearing loss. Based on
presenting symptoms, diagnosis ma be made by visual examination or b
computed tomography (CT) or MRI. Therapy includes treatment of the acute
infection and surgical removal of the mass to restore hearing.
MEDICAL MANAGEMENT
• Local treatment of chronic otitis media consists of careful suctioning of the ear
under otoscopic guidance.
• Instillation of antibiotic drops or application of antibiotic powder is used to treat
purulent discharge.
• Systemic antibiotics are prescribed only in cases of acute infection.

SURGICAL MANAGEMENT
• Surgical procedure, including tympanoplasty, ossiculoplasty, and
mastoidectomy, are used if medical treatments are ineffective.
• TYMPANOPLASTY
• The most common surgical procedure for chronic otitis media is a
tympanoplasty, or surgical reconstruction of the tympanic membrane.
• Reconstruction of the ossicles may also be required.
• The purpose of a tympanoplasty are to be reestablished middle ear function,
close the perforation, prevent recurrent infection, and improve hearing.
• There are five tpes of tympanoplasties.
• Type I (myringotomy) the simplest surgical procedure designed to close the
perforation in the tympanic membrane.
• Type II-V involve more extensive repair of the middle ear structures.
• The structures and the degree of involvement can differ, but all tympanoplasty
procedures include restoring the continuity of the sound conduction
mechanism.
• Tympanoplasty is performed through the external auditory canal with a
transcanal or through a postauricular incision.
• The contents of the middle ear are carefully inspected, and the ossicular chain
Malleus and incus unit) is evaluated.
• Ossicular interruption is most frequent in chronic otitis media, but problems are
reconstruction can also occur with malformations of the middle ear and
ossicular dislocations due to head injuries.
• Dramatic improvement in hearing can result from closure of a perforation and
reestablishment of the ossicles.
• Surgery is usually performed in an outpatient facility under moderate sedation
or general anesthesia.

OSSICULOPLASTY
• Ossiculoplasty is the surgical reconstruction of the middle ear bones to restore
hearing.
• Prostheses made by materials such as teflon, stainless steel, and
hydroxypatite are used to reconnect the ossicles, thereb reestablishing the
sound conduction mechanism.
• However, the greater the damage, the lower the success rate for restoring
normal hearing.

MASTOIDECTOMY
• The objective of mastoid surgery are to remove the cholesteatoma, gain
access to the diseased structures, and create dry (noninfected) and healthy
ear.
• If possible, the ossicles are reconstructed during the initial surgical operation.
• A mastoidectomy is usually perormed through a postauricular incision.
• Infection is eliminated by removing the mastoid air cells.
• A second mastoidectomy may be necessary to check for recurrent or residual
cholesteatoma.
• The hearing mechanism ma be reconstructed at this time.
• The success rate for correcting the conductive hearing loss is approximately
75%.
• Surgery is usually performed in an outpatient setting.
• The patient has a mastoid pressure dressing, which can be removed 24-48
hours after surgery.
• Although infrequent injure, the facial nerve, which runs through the middle ear
and mastoid, is at some risk for injury during surgery.
• As the patient awakens from anesthesia, any evidence of facial paresis should
be reported to the physician.

Pathophysiology
• Eustachian tube dysfunction is thought to be the primary cause of otitis media.
• Two major types of ET obstruction can lead to pathologic changes in the
middle ear.
• Functional obstruction results from collapse of the ET due to increased tubal
compliance or an abnormal active opening mechanism.
• This type of obstruction is common in infants and younger children due to a
decrease in the the amount and stiffness of the cartilage supporting the ET.
• Also, the tensor veli palatini muscle is less efficient before puberty due to age
related differences in the skull base.
• Mechanical obstruction may be either intrinsic or extrinsic.
• Intrinsic obstruction may result from abnormal geometry or intra- or extra-
luminal factors which compromise the lumen.
• Most commonly this is due to inflammation from infection or allergy. Extrinsic
obstruction may be due to extramural pressure from a supine position or from
tubal compression related to a mass - for example the adenoids or tumor.
• With ET obstruction oxygen and nitrogen within the middle ear is reabsorbed
leading to the development of a relative negative pressure.
• The rate of resorption of gases from the middle ear is reported to be about
1cc/24 hours.
• This negative pressure leads to transudation of fluid and resultant edema of
the muco-periosteum.
• This transudate occurs as a passive transfer of serous fluid from the
subepithelial vessels.
• Infection, persistent effusion and epithelial damage promote the release of a
number of potent inflammatory mediators.
• Together with the presence of bacterial toxins and enzymes and an increase in
the partial pressure of CO2, these mediators stimulate metaplasia of the ET
and middle ear epithelium to a more secretory type characteristic of the lower
respiratory tract.
• There is an increase in mucus producing goblet cells and enlargement of the
subepithelial glands with a resultant increase in production of mucous to
protect the irritated epithelium.
• Abnormalities of the mucociliary blanket result.
• As the blanket becomes too thick cilia do not penetrate the mucous and their
effectiveness is reduced.
• Production of tenacious mucous may cause adherence of the mucous blanket,
anchoring it in place, and preventing the secretion of a less viscous mucous.
• In extreme cases, an abnormally patulous tube may be open even at rest,
lesser degrees of abnormal patency may result in a semi- patulous ET that is
closed at rest but has a lower opening resistance than a normal ET.
• This can result in failure to protect the middle ear from nasopharyngeal
secretions and can result in "reflux otitis media".
• American Indians and Eskimos have been found to have abnormally patent
ET.
• Various other factors have been associated with the development of
otitis media with effusion:
• Viral infection is frequently associated with otitis media.
• Researchers have demonstrated a correlation between isolation of viruses
from the upper respiratory tract and the clinical diagnosis of otitis media.
• OM was increased in the 14 days following upper respiratory isolation of RSV,
adenovirus, influenzae a and b, mumps and enterovirus.
• RSV has further been shown to induce a state of IgE-mediated hypersensitivity
in the nasopharynx.
• Bacterial infection is felt to be predominantly secondary to viral infection.
• Viruses are infrequently cultured from the middle ear in otitis media.
• Adenoids are rarely large enough themselves to cause mechanical
obstruction but the obstruction of lymphatics draining the middle ear and ET
may be a factor of greater importance.
• Chronic adenoiditis may provide a focus of pathogenic bacteria adjacent to the
tubal orifice.
• Gates found no correlation between the size of the adenoid pad and resolution
of COME after adenoidectomy - therefore the main benefit of adenoidectomy
may be the reduction in the bacterial flora of the nasopharynx.
Allergy: Multiple studies have tried with varying success to prove or disprove an
allergic effect on the ME mucosa and eustachian tube.
• Friedman showed that a provocative intranasal pollen application produced
allergic rhinitis followed by ET obstruction, and that allergic reactions in the
nose and nasopharynx inhibit even transient dilatations of the ET tube during
swallowing. Bernstien found that in 15% of children with proven allergy, there
was evidence of the middle ear as a target organ.
• The exact method by which allergy affects ET function is elusive, but three
different immunologic mechanisms may play a role in the pathogenesis of
COME:
• IgE mediated hypersensitivity - Bernstein et al demonstrated the
independent local production of nasal and middle ear IgE.
• Immune complexes - studies suggest these do occur in the middle ear but
are felt to represent normal immuno-elimination of bacteria and viruses rather
than being pathologic for the middle ear mucosa.
• Delayed hypersensitivity - macrophages and lymphocytes predominate in
chronic middle ear effusions.
• Perivascular infiltration of mononuclear cells is classic for delayed
hypersensitivity and is often seen in COME.
• Sinusitis - chronic sinus infection often times parallels similar process within
the middle ear.
• Cleft palate is almost universally associated with COME in children with
unrepaired clefts, probably due to functional obstruction of the ET.
• Submucous clefts appear to have the same risk for COME, and there is a high
incidence of OM in children with bifid uvulae.
• Studies have demonstrated that the ETs of patients with cleft palates constrict
instead of dilating during swallowing.
• Tumors - a unilateral middle ear effusion in an adult is tumor until proven
otherwise.

OTOSCLEROSIS
• Otosclerosis involves the stapes and is thought to result from the formation of
new, abnormal spongy bone, specially around the oval window; with resulting
fixation of the stapes.
• The efficient Transmissions of sound is prevented because the stapes cannot
vibrate and carry the sound as conducted from the malleus and incus to the
inner ear.
• It is more common to women and frequently hereditary, and pregnant women
may worsen it.

CLINICAL MANIFESTATIONS
• Otosclerosis may involve one or both ears and manifested as a progressive
conductive or mixed hearing loss.
• The patient may or may not complain of tinnitus.
• Otoscopic examination usually reveals a normal tympanic membrane.
• Bone conduction is better than air conduction on Rinne’s testing.
• The audiogram confirms conductive hearing loss or mixed loss, especially in
the low frequencies.

TREATMENT
• Medical therapy: As with conductive hearing losses of other etiologies,
hearing aids are usually helpful.
• Fluoride supplementation has met with variable response and is used
sporadically for labyrinthine otosclerosis.
• It has also been used for postoperative medical management of obliterative
otosclerosis.
• Surgical therapy:
 total stapedectomy,
 partial stapedectomy,
 stapedotomy.

MIDDLE EAR MASSES

MIDDLE EAR SCHWANNOMAS

Pathophysiology
• Schwannomas have been identified along the entire course of the facial nerve,
although intratemporal tumors appear to be much more common than
intracranial tumors.
• Within the temporal bone, the most common sites of involvement, in
descending order, are the geniculate ganglion, horizontal and vertical
segments, internal auditory canal, and labyrinthine segment.
• A small percentage of schwannomas display an unusual multicentricity
evidenced by multiple discrete intraneural connections, sometimes described
as a string of pearls.
• The tumors tend to grow longitudinally along the lumen of the fallopian canal
and may prolapse into the middle ear and out of the stylomastoid foramen.
• Primary schwannomas of the middle ear may arise from the facial nerve,
chorda tympani, or the Jacobsen nerve.
• In contrast to the more commonly appearing vestibular schwannoma (ie,
acoustic neuroma), facial nerve schwannomas tend to grow at a slower rate
and are often present for years before detection.
• Because of the facial nerve's intimate relationship with the sensory organs, otic
capsule erosion is more common in facial nerve schwannomas, occurring in as
many as 30% of patients.

Clinical presentation
• Facial nerve dysfunction (eg, palsy, twitch) is the hallmark of clinical
presentation and is evident on clinical examination in 25-50% of patients.
• Nerve compression within the fallopian canal causes facial nerve disfunction.
• The most common pattern is slowly progressive palsy, often accompanied by
hyperfunction manifested as limited twitch or full hemifacial spasm.
• Recurrent acute paralytic episodes with partial or complete recovery may also
occur. Patients are commonly misdiagnosed with Bell palsy with the first
episode of paralysis. Successive bouts of palsy then ensue, with increasingly
poorer facial nerve function. This presentation of recurrent increasingly severe
episodes of facial palsy is a classic characteristic of facial nerve schwannoma.
• The facial nerve is surprisingly resistant to compression.
• An estimated 50% of facial nerve fibers must degenerate before clinical signs
of palsy are detected. In one study of 48 patients with facial nerve neuromas,
26 presented with normal facial function.
• Patients without functional recovery from an idiopathic facial paralysis after 3
months or with a history of recurrent Bell palsy should undergo enhanced MRI
to search for tumor or facial nerve pathology.
• Patients may also present with normal facial nerve function and conductive
hearing loss. A surgeon performing an exploratory tympanotomy for conductive
hearing loss may occasionally encounter a small facial nerve schwannoma
impinging upon the stapes bone and oval window.
• This condition leads to a hearing loss similar to that observed in otosclerosis.
• Additional presenting symptoms include vertigo from a labyrinthine fistula and
sensorineural hearing loss from cochlear invasion.
• Prolonged pain should also raise suspicion for a diagnosis other than
idiopathic facial palsy.
• Ear examination may demonstrate a mass behind the drum in as many as
29% of patients.

Diagnosis
• Facial nerve schwannomas are often found incidentally during routine middle
ear or mastoid surgery.
• Since biopsy of a facial nerve schwannoma in the middle ear usually results in
facial paralysis, appropriate imaging studies are recommended prior to
obtaining a biopsy of any middle ear tumor.
• In cases of a facial nerve schwannoma, temporal bone CT scan typically
reveals enlargement of the fallopian canal along its length.
• Ossicular erosion and involvement of the horizontal semicircular canal may
also be revealed; however, these findings are nonspecific and may also be
present in other middle ear pathologic conditions such as paraganglioma and
cholesteatoma.
• MRI better characterizes the lesion, which appears hypointense on T1-
weighted images, hyperintense on T2-weighted images, and shows marked
enhancement with gadolinium dye.
• An enhancing enlargement of varying thickness along a large segment of
facial nerve is considered highly suggestive of schwannoma.
• While high-resolution CT scanning can reveal these tumors because of their
osseous erosion, MRI is a more sensitive diagnostic tool.
• However, both modalities are useful for surgical planning.
• Site-of-lesion tests (eg, Schirmer test of lacrimation, stapedial reflex testing),
while theoretically attractive, are not completely reliable and have become
largely obsolete because of the availability of CT scan and MRI.

Treatment
• Treatment for facial nerve schwannomas is primarily surgical.
• Although a conservative approach is warranted at times for lesions limited to
the transverse or descending portions of the nerve, a tympanomastoid
approach may be used.
• Lesions that also involve the labyrinthine segment of the facial nerve, internal
auditory canal, or geniculate ganglion require the addition of an extradural
middle cranial fossa approach.
• If cochlear function has been destroyed, then a translabyrinthine approach
may be used.
• Occasionally, removing a facial nerve schwannoma with preservation of its
nerve of origin is possible.
• However, more commonly, nerve repair with an interposition graft is necessary.
• This is typically accomplished with a greater auricular or sural nerve graft. In
general, patients with long-standing facial nerve paralysis tend to have poorer
postoperative facial nerve function.
• The decision of when to remove a facial nerve neuroma depends upon a
number of factors.
• The advantages of removing the tumor early, while it is small, include
assurance that the tumor is completely resected with the least likelihood of
injuring adjacent structures, including the hearing and balance organs.
• Additionally, a maximum number of surviving healthy neurons for grafting the
nerve are available.
• However, the principle disadvantage of removing the tumor early is that the
patient often has good nerve function in this situation, and tumor removal
nearly always destroys residual nerve function.
• Further, grafting a transected nerve never results in facial function better than
a grade III/VI (House-Brackmann Grading Scale).
• Thus, many surgeons take a middle-of-the-road approach by delaying surgery
until facial nerve function has deteriorated beyond a grade III/VI.
• However, surgery should be instituted sooner if adjacent structures are in
jeopardy (ie, CNS, inner ear organs), any question exists regarding the
diagnosis, or the tumor is growing rapidly.
• GLOMUS TYMPANICUS TUMORS
• Introduction
• The most common tumor of the middle ear and second most common tumor
found in the temporal bone is the paraganglioma, commonly referred to as the
glomus tumor. Chemodectoma is another term occasionally used to describe
this tumor.
• Glomus tumors originate in the paraganglia, which exist throughout the
temporal bone, including on the jugular dome, the promontory of the middle
ear, and along the Jacobson and Arnold nerves.
• This anatomy accounts for the predilection of glomus tumors toward these
anatomic sites.
• The term glomus was associated with these tumors when their origin was
believed to be similar to true glomus (arteriovenous) complexes.
• Despite being a misnomer, the nomenclature has persisted.
• Glomus tumors involving the temporal bone are divided into two categories,
based on their anatomic location.
• Those arising along the course of the Jacobson nerve and involving primarily
the tympanic cavity are termed glomus tympanicum.
• Paragangliomas arising from the dome of the jugular bulb and involving the
jugular foramen and related structures are termed glomus jugulare.
• Both types are marked by slow, progressive growth, spreading via the
pathways of least resistance (eg, temporal bone air cell tracts, neural
foramina, vascular channels, bony haversian systems, eustachian tube).
• Pathophysiology
• While most glomus tumors appear to arise sporadically, familial disease has
been reported with an unusual genomic imprinting mode of inheritance.
• In this manner of transmission, tumors only occur in the offspring of an
affected female when the gene is transmitted through a carrier male.
• This accounts for the observed tumor occurrence in skipped generations.
• A clear predilection for these tumors is found in females, and patients usually
present after the fifth decade of life.
• Glomus tumors are typically reddish purple, vascular lobulated masses.
• Histologically they resemble normal paraganglia with clusters of chief cells,
characteristically termed zellballen (the literal German translation is "cell balls")
in a highly vascular stroma.
• This pattern is enhanced on silver staining, which is useful diagnostically.
• Sustentacular cells and nerve axons, seen in the normal paraganglion, rarely
appear in the tumor.
• Clinical presentation
• Because of the vascularity of these tumors, pulsatile tinnitus is often the first
presenting symptom.
• Further growth causes conductive hearing loss as ossicular mobility is
inhibited. Hearing loss is present in approximately half of patients.
• Continued expansion may cause the tumor to erode laterally through the drum,
mimicking a friable bleeding polyp, or it may expand medially, causing facial
nerve dysfunction, sensorineural hearing loss, or vertigo.
• In a large series of 71 patients, presenting symptoms, in order of decreasing
frequency, were pulsatile tinnitus (76%), hearing loss (conductive 52%, mixed
17%, sensorineural 5%), aural pressure/fullness (18%), vertigo/dizziness (9%),
external canal bleeding (7%), and headache (4%).
• The Brown sign, which consists of a pulsatile purple-red middle ear mass that
blanches with positive pneumatic otoscopy, is a frequently mentioned
distinguishing sign but is of little clinical value.
• Diagnosis
• Differentiation between glomus tympanicum and jugulare tumors is not always
possible by physical examination alone since both lesions typically involve the
middle ear.
• Furthermore, other vascular lesions of the middle ear (eg, aberrant carotid
artery, high-riding jugular bulb) may mimic a glomus tumor; thus, radiographic
evaluation prior to biopsy or surgical intervention is important.
• A temporal bone CT scan with a contrast-enhancing mass limited to the middle
ear at the level of the cochlear promontory with an intact plate of bone at the
lateral aspect of the jugular fossa suggests the diagnosis of glomus
tympanicum.
• CT scanning is also useful for evaluating the degree of bony erosion and the
tumor's relationship to surrounding temporal bone structures.
• MRI, though not as helpful as CT scanning in evaluating bony changes within
the temporal bone, is superior in identifying the extent of the tumor and
defining the relationship of the tumor to surrounding structures once it has
extended beyond the confines of the middle ear.
• Because the middle ear mass could be the tip of a larger glomus jugulare
invading the middle ear from the jugular foramen, both CT scan and MRI are
critical components of the diagnosis.
• The appearance of a paraganglioma on MRI reflects its highly vascular nature.
Glomus tumors are isointense on T1-weighted images and brightly enhance
with gadolinium.
• They typically possess numerous signal voids due to the numerous vascular
channels within them. On T2-weighted images, they demonstrate increased
signal intensity in the solid portions of the tumor with persistent flow void in the
vascular portions.
• The characteristic salt-and-pepper pattern secondary to punctuate flow voids
seen in larger paragangliomas is not appreciated in tumors smaller than 2 cm.
• Some advocate that the imaging study be carried down to the level of the
carotid bifurcation to determine if multiple tumors exist.
• If the lesion is extensive, angiography may help further evaluate glomus
tumors, but it should be deferred until the preoperative period, when both
diagnostic and therapeutic (embolization) measures can be accomplished in a
single study.
• Angiography allows determination of arterial supply, degree of vascularity,
degree of arteriovenous shunting, evidence of major venous sinus occlusion,
and confirmation of the diagnosis.
• It can evaluate the right, left, internal, and external carotid systems for
evidence of multiple early lesions with a single study.
• Embolization is usually performed at the time of angiography as a preoperative
maneuver to limit surgical blood loss.
• Because of the limited size and extent of most glomus tympanicum tumors,
angiography and embolization are rarely necessary.
• Magnetic resonance angiography and venography are newer modalities that
can also aid in the diagnosis of vascular lesions of the temporal bone,
including glomus tumors.
• The role of these newer radiographic modalities in the evaluation of glomus
tumors is still being defined.
• As previously stated, angiography, while useful for larger lesions, is not
required for small glomus tympanicum tumors limited to the middle ear that
can occasionally be visualized by less invasive techniques such as magnetic
resonance angiography.
• Treatment
• Surgery is the principle mode of therapy for glomus tympanicum tumors.
• Small lesions limited to the promontory that can be visualized completely by
otoscopy and are confined to the mesotympanum on a CT scan result can be
approached via a transcanal incision and a tympanomeatal flap to expose the
middle ear.
• Recently, some authors have advocated the use of the diode or potassium
titanyl phosphate (KTP) laser for tumor resection.
• Larger lesions are best exposed postauricularly via an extended facial recess
approach. Extremely large lesions may need to be approached via an
infratemporal fossa approach, similar to a glomus jugulare.
• Using these methods, complete tumor removal can be achieved in more than
90% of patients. Closure of the air-bone gap can be expected in most patients,
while approximately 10% experience some sensorineural worsening.
• For poor surgical candidates, radiotherapy alone may be an option.
• Although radiation therapy does not eradicate the tumor, good local control
and symptomatic relief may be achieved without significant morbidity.
• ADEMATOUS TUMORS
• Introduction
• Adenomatous tumors involving the temporal bone are rare lesions, with slightly
more than 100 cases reported in the English-language literature over the past
century.
• Historically, all adenomatous tumors of the middle ear and temporal bone have
been confusingly grouped together.
• However, recently, two distinct clinical and histopathological subtypes have
been identified: a mixed pleomorphic cell pattern and a papillary pattern.
• Carcinoid tumors are also recognized by some as a distinct clinical subtype of
adenomatous tumor, though others group these tumors with the mixed
pleomorphic cell type.
• Adenomatous tumors also include some lesions that previously have been
reported as ceruminomas, an ambiguous and misleading term used to
describe a diverse group of glandular tumors of the middle ear and mastoid.
• Mixed pleomorphic cell pattern (mucosal adenoma)
• Mixed tumors are the more common and benign of the two major subtypes of
adenomas and are always confined to the middle ear and mastoid.
• This pattern demonstrates acinar, solid and trabecular, and carcinoidlike
histopathologic features. Some bone involvement is always present, and
cholesteatoma or inflammation is nearly always present.
• The otic capsule or facial nerve may be involved in rare cases.
• These tumors are believed to arise from the poorly differentiated basement
membrane cells within the normal mucosa of the middle ear, promontory, and
eustachian tube.
• Clinical presentation
• Most patients with mixed pleomorphic tumors of the middle ear are male and
typically present between ages 20 and 60 years.
• Mixed tumors are commonly diagnosed during evaluation of chronic otitis
media.
• Conductive hearing loss is often present as a result of tumor growth occluding
the sound-transducing mechanism, while otorrhea, cranial nerve VII
weakness, and tinnitus are variably present.
• Examination typically demonstrates a soft tissue middle ear mass.
• Evaluation and treatment
• High-resolution CT scans add to the clinical examination and usually
demonstrate a soft tissue middle ear and mastoid mass without associated
bone destruction.
• Because these lesions are commonly confused with chronic otitis media, the
diagnosis is rarely made preoperatively; it is typically made during a routine
mastoidectomy.
• Despite the benign implication of its diagnosis, a mixed pleomorphic pattern
tumor has a high likelihood of recurrence with the ability to invade bone and
soft tissue.
• Thus, complete surgical resection is necessary for cure, and long-term follow-
up care is mandatory to evaluate for recurrence.
• Papillary pattern (endolymphatic sac adenoma)
• Adenomatous tumors with a papillary pattern are more rare and more
aggressive lesions than pleomorphic middle ear adenomas. Approximately 39
have been reported in the English-language literature.
• Historically, these lesions have also been termed endolymphatic sac tumors,
Heffner tumors, low-grade papillary adenocarcinoma, and aggressive papillary
middle ear tumors.
• In contrast to their more benign counterpart, papillary neoplasms typically
demonstrate adjacent bone invasion and extension into the petrous apex.
• Involvement of the facial nerve and middle or posterior cranial fossa dura is
also common.
• These tumors are believed to originate in the endolymphatic sac and
subsequently extend into the posterior fossa and endolymphatic duct,
providing access to the vestibule, mastoid process, and retrofacial air cells and
facial nerve.
• However, limited evidence suggests the tumors may arise from the mucosa of
the pneumatic spaces surrounding the jugular bulb.
• Histologically, these tumors are composed of a single- or double-layered
epithelial lining with a variable cytoplasm and hyalinization.
• All papillary tumors invade adjacent bone and demonstrate glandular features
that suggest they originate in the endolymphatic sac.
• Clinically, these tumors may behave aggressively and have a lethal potential.
• These tumors have a predilection for females, and patients usually present
when aged 20-60 years. Symptoms at presentation include hearing loss, facial
nerve paralysis, vertigo, and tinnitus.
• On high-resolution CT scanning, the lesions are typically located near the
vestibular aqueduct, centered between the sigmoid sinus and the internal
auditory canal.
• Involvement of the internal auditory canal, jugular bulb, and mastoid are
common, as is erosion of the bone toward the vestibule of the labyrinth.
• Treatment is primarily surgical, with complete excision and adequate margins
the surgical goals. These goals are usually accomplished via a
translabyrinthine approach that removes the dura, jugular bulb, and any
involved cranial nerves.
• Postoperative radiation is controversial since debate remains regarding
whether the tumor is malignant or benign.
• It displays clinical and pathologic features of both states. With gross total
surgical removal, a 90% cure rate has been reported.
• When radiation therapy is used after incomplete tumor extirpation, only 50% of
tumors respond, although the numbers reported are very small and not
statistically valid.
• Carcinoid tumor
• While some believe that all carcinoid tumors of the middle ear should be
classified as mixed pleomorphic adenomatous tumors, others consider them to
be a unique histopathological subtype of adenomatous tumors.
• Approximately 46 cases have been reported in the English-language literature
since the first description.
• Carcinoid tumors are slow-growing but locally invasive lesions found in the
middle ear.
• These rare lesions are believed to arise from the enterochromaffin cells of the
endocrine system and thus have the ability to secrete a variety of peptide
hormones.
• However, unlike similar lesions in other parts of the body, middle ear carcinoid
tumors do not secrete large amounts of these hormones and thus are not
associated with the systemic manifestations of carcinoid syndrome (eg,
flushing, wheezing, abdominal cramps, diarrhea). Only one case of carcinoid
syndrome due to a neuroendocrine tumor of the middle ear has been reported.
• Histologically, these tumors demonstrate ribbons and cords of trabecular
cuboidal cells. Argyrophil staining is positive in 80% of cases.
• Immunohistochemical stains are positive for AE-1, AE-3, serotonin, and
neuron-specific enolase. Electron microscopy demonstrates neurosecretory
granules.
• Clinical presentation
• Tumors manifest in both sexes between the second and sixth decades.
• Patients typically present with conductive hearing loss, aural fullness, and
tinnitus.
• Transient facial paresis has also been described.
• Otologic examination may reveal a red or pale mass behind an intact tympanic
membrane or a bulging red tympanic membrane.
• A middle ear mass is visible in less than half of patients.
• CT scanning is useful in identifying the extent of middle ear involvement and
the status of the ossicles and facial nerve.
• Bone erosion or destruction is never observed with carcinoid tumors.
• Treatment
• Definitive therapy involves complete tumor excision.
• Because the ossicles are frequently enveloped by tumor and extend into the
mastoid, the surgeon should be prepared to perform tympanomastoidectomy
concurrent with ossicular reconstruction.
• With adequate excision, surgical treatment provides good long-term control.
• In a recent review of 46 patients who were undergoing surgery for middle ear
carcinoid tumors, the overall recurrence rate was 22%.
• On average, recurrence occurred 11 years after treatment but ranged from 13
months to 33 years.
• Chemotherapy, somatostatin analogues, and radiation have been used in the
treatment of gastrointestinal and pulmonary carcinoid tumors; however, data
on the efficacy of these alternative treatment options are not available for
carcinoid tumors of the middle ear.
• Glandular tumors of the external auditory canal
• The general term ceruminoma has been applied to a diverse spectrum of
tumors originating from the glandular structures of the external auditory canal.
• The rarity of these lesions has contributed to the confusion.
• The most extensive review of the topic cites only 32 cases over a 32-year
period.
• These tumors represent a variety of glandular tumors ranging from benign to
malignant.
• The benign tumors include ceruminous adenomas similar to the mixed-
pleomorphic pattern of the middle ear; pleomorphic adenomas, which are
salivary gland Choristomas; and cylindromas, exceedingly rare tumors arising
from the pilosebaceous units of the external canal.
• The malignant varieties of glandular tumors, which have also been termed
ceruminomas of the external auditory canal, include adenoid cystic
carcinomas, ceruminous adenocarcinomas, and mucoepidermoid carcinomas.
• Manifestation of the benign ceruminous adenoma typically includes external
auditory canal obstruction with hearing loss.
• Treatment involves conservative local excision with a skin graft to the
operative site. Radiotherapy is not necessary.
• Choristoma is the pathological term given to a benign cohesive mass of
aberrant tissue or scattered cells in an inappropriate anatomic location.
• While most reports address salivary gland choristomas, neural and sebaceous
choristomas have also been described.
• Choristomas are extremely rare in the temporal bone; less than 30 cases of
middle ear choristomas have been reported in the English-language literature.
• One theory on the development of middle ear choristoma is that salivary gland
tissue becomes trapped during the embryonic fusion of the tympanic, mastoid,
and squamous portions of the temporal bone, leading to the formation of
salivary choristomas.
• Neural rests of tissue are believed to gain access to the middle ear via Hyrtl
(tympanomeningeal) fissures during development, giving rise to the less
common neural choristoma.
• Pathophysiology
• Microscopically, choristomas of the middle ear are characterized by well-
formed serous and mucous acini arranged randomly or in a lobular formation.
• Mucinous microcysts and fibroadipose tissue components have also been
described. Macroscopically, the tumors are lobulated and firm.
• Occasionally the tumor is attached to the middle ear by a fine stalk.
• Choristomas typically arise in the posterosuperior tympanum, although they
vary in size and may fill the entire tympanic cavity.
• They are frequently associated with ossicular anomalies, particularly an absent
or malformed incus or stapes. Facial nerve dehiscence or displacement is also
common.
• Because of this frequent association, a second branchial arch embryologic
etiology has been proposed.
• Clinical presentation and treatment
• Choristomas have been reported in individuals aged 11 months to 52 years,
and no sex predilection is described.
• They are typically unilateral, although bilateral involvement has been reported.
• These benign tumors grow slowly and tend to produce few symptoms other
than a conductive hearing loss in the affected ear correlating with the degree
of ossicular involvement.
• Serous otitis media was seen in 24% of patients, according to one review.
• Treatment is determined by the size and location of the tumor. Small tumors or
those attached solely by a thin stalk may be readily excised.
• However, larger or broad-based tumors must be approached with a degree of
caution.
• Because of the frequent association of choristomas with the facial nerve,
temporary or permanent palsy has been reported in 25% of patients after
tumor resection.
• Ossiculoplasty has been successful in correcting conductive hearing loss in
approximately two thirds of patients.
• Because little-to-no tumor growth often occurs over time and no evidence of
malignant degeneration is reported with middle ear choristomas, conservative
management with serial examinations is acceptable for those wishing to forego
surgery.
• HEMANGIOMAS AND VASCULAR MALFORMATIONS
• Historically, the literature on benign vascular tumors has lacked a rational or
consistent nomenclature and has contributed to widespread misunderstanding
of these lesions.
• The term hemangioma has often been used to describe any vascular lesion
and is commonly preceded by descriptive but confusing and unhelpful terms,
such as strawberry, cavernous, and capillary.
• In 1982, a new system of classification of vascular tumors was developed
based upon the clinical behavior and growth characteristics of these lesions.
• The classification groups vascular tumors into two categories, hemangiomas
and vascular malformations.
• Hemangiomas usually manifest during the first month of life and are
characterized by a rapid growth period (proliferative phase) followed by a slow
period of involution.
• Hemangiomas are categorized further on the basis of depth within the dermis
into cutaneous (ie, entirely within papillary dermis), subcutaneous (ie, into the
reticular dermis or subcutaneous fat), or compound, which contains elements
of both. Only 10 cases of isolated middle ear hemangiomas have been
reported in the literature.
• In contrast, vascular malformations are always present at birth and grow in
proportion to body growth without regression.
• They can be arterial, capillary, venous, lymphatic, or any combination.
• Some have further divided these vascular malformations into low-flow lesions
(venous malformations) and high-flow lesions (arteriovenous malformations).
• Unfortunately, even recent otologic literature does not differentiate between
these 2 types of lesions, which makes clinical comparisons difficult.
• To add a further element of confusion, some have reported that vascular
lesions of the temporal bone frequently contain elements of both
hemangiomas and vascular malformations.
• However, most vascular lesions of the temporal bones are probably
subcategories of vascular malformations.
• Vascular malformations of the temporal bone are rare entities, comprising
fewer than 1% of all temporal bone tumors.
• Histology and pathophysiology
• Histologically, hemangiomas are characterized by endothelial hyperplasia and
an increase in the number of mast cells during the proliferative phase, followed
by fibrosis, fatty infiltration, decreased cellularity, and normalization of the mast
cell count during involution of the lesion.
• In contrast, vascular malformations are collections of abnormal vessels with
normal endothelium and mast cell counts.
• Using these histologic criteria, lesions commonly identified by the term
cavernous hemangioma are more appropriately classified as vascular
malformations.
• Alternatively, the term capillary hemangioma describes a true hemangioma,
but as some authors have indicated, these have not been reported in the
temporal bone.
• The overwhelming majority of vascular malformations manifest within the
internal auditory canal or at the geniculate ganglion.
• In rare cases, they may arise within the middle ear.
• The extensive blood supply surrounding Scarpa ganglion and the geniculate
ganglion make this region relatively hospitable to tumors.
• Most tumors are smaller than 1 cm at the time of presentation.

Clinical presentation
• Patients typically present between the third and seventh decades of life.
• When the geniculate ganglion is the site of origin, a cranial nerve VII
dysfunction (ie, weakness, twitch, or both) is nearly always present.
• Overall, facial nerve dysfunction is present in approximately 80% of temporal
bone vascular malformations and is usually the reason patients seek medical
attention.
• Other symptoms noted on clinical presentation include tinnitus, conductive
hearing loss (more common with geniculate ganglial malformations),
progressive sensorineural hearing loss (more common with internal auditory
canal tumors), and vertigo.

Imaging studies
• High-resolution CT scanning or MRI reveals the lesion and provides
complimentary information. MRI demonstrates all tumors within the internal
auditory canal and some tumors near the geniculate.
• The lesions appear hyperintense on T2-weighted images and tend to be more
hyperintense than acoustic schwannomas.
• Some geniculate ganglion lesions are difficult to visualize on MRI, but
intratumoral calcium can be detected on a high-resolution CT scan.
• Venous malformations of the geniculate region may be differentiated from
other temporal bone tumors based upon radiographic appearances.
• A focal, enhancing lesion of the geniculate ganglion that is sessile upon the
middle fossa floor, erodes bone diffusely, has irregular margins, and contains
flecks of calcification is most likely a meningioma.
• Facial nerve schwannomas typically cause smoothly marginated expansion
and tend to be less focal, extending along the fallopian canal longitudinally.
Treatment
• Treatment of choice is surgical excision with removal of normal bony margins
by drill. The choice of surgical approach depends on tumor location and size,
but middle-fossa, transmastoid, and translabyrinthine approaches are
commonly used.
• Because of the destructive nature of these benign tumors, intratemporal facial
nerve grafting is frequently required.
• Facial nerve repairs are required more often for geniculate vascular
malformations than for those originating within the internal auditory canal.
• When facial paralysis is of recent origin or when partial function remains, the
native facial nerve can often be preserved.
• However, in long-standing complete palsies, a graft is almost always required.
• Surgery is generally successful at eradicating lesions, with a low likelihood of
recurrence after complete excision.
• Results of facial nerve function following repair are good (ie, House-
Brackmann grade II-IV/VI) except when nerve repair is delayed more than 1
year from the onset of the palsy. Approximately two thirds of patients
undergoing middle fossa or transmastoid procedures can expect postoperative
hearing preservation to within 10 dB of preoperative speech thresholds.
 Aural Rehabilitation

- The purpose of aural rehabilitation is to maximize the hearing impaired

person’s communication skills; it includes auditory training, speech training
and the use of hearing aids and hearing dogs
1. AUDITORY TRAINING – emphasizes listening skills, so the hearing
impaired person concentrate’s on the speaker
2. SPEECH TRAINING – (formally known as lip reading) help fill the gaps left
by missed or misheard word
- it attempts to conserve, develop and prevent deterioration of current skills
3. HEARING AIDS – a device through which speech and environmental
sounds are received by microphone, converted to electrical signals
amplified and reconverted to the acoustic signals
- a general guideline for assessing the pts. Need for a hearing aid is a
hearing loss exceeding 30dB in the range of 500 – 2000 H2 in the better
hearing ear

“ Health care professionals who dispense hearing aid’s are required to better
prospective user’s to a physician if any of the following otologic conditions are
evident::”
1. Visible congenital or traumatic deformity of the ear
2. Active drainage from the ear with in the previous 90 days
3. Sudden or rapidly progressive hearing loss with in the previous 90 days
4. Complaints of dizziness or tinnitus
5. Unilateral hearing loss that occurred suddenly or with in previous 90 days
6. Audiometric air/bone gap of 15db or more at 500, 1000, 2000 H2
7. Significant accumulation of cerumen or a foreign body in the external
auditory canal
8. Pain or discomfort in the ear

IMPLANTED HEARING DEVICE

3 Types of implanted hearing device are either currently available or in the

investigational stage

1. THE COCHLEAR IMPLANT

 for patients with little or no hearing
 it is an auditory prosthesis used for people with profound
sensoneural hearing loss bilaterally who do not benefit from
conventional hearing aids
  it is design to provide stimulation directly to the auditory nerve by
passing the hair cells of the inner ear which are not functioning
 the microphone or signal processor are worn outside the body to the
implanted electrodes the electrical signals stimulate the auditory
nerve fibers and then the brain, where they are interpreted

- an implant is does not restore normal hearing, rather it helps the person
detect medium to loud environmental sound and conversation
- The hearing loss can be congenital or acquired
- Candidate for cochlear implant:
1. at least 1 year old careful screening by otologic history, physical
exam audiologic testing and x-rays psychological testing

- Criteria for adults that may benefit from COCHLEAR IMPLANT:

Profound sensoneural hearing loss in both ears
Inability to hear and recognize speech well with hearing aids
No medical contraindications to a cochlear implant or general
anesthesia
Indications that being able to hear would enhance the
patients life

2. Bone conduction device:

 transmits sound through the skull to the inner ear used in patients
with a conductive hearing loss if hearing aid is contraindicated (ie.
Those with chronic infection)
 is implanted post auricularly under the skin into the skull and an
external device worn above the ear

3. Semi implanted hearing aids

 Is not yet approved by the food and drug administration
except in testing sites

HEARING GUIDE DOGS

Specially trained dogs are available to assist person with a
hearing loss
People who live alone are eligible to apply for a dog trained
by International Hearing Dog, Inc.
At home the dog reacts to the sound of a telephone, doorbell,
alarm clock a baby’s cry, knock at the door, smoke alarm or
an intruder
The dogs does not bark but alerts its master
 CERUMEN IMPACTION

- it normally accumulates in the external canal in various amounts and

colors.

Pathophysiology:
- Cerumen normally accumulates in the external canal in various amounts
and colors. Although wax does not usually need to be removed, impaction
occasionally occurs causing otalgia(a sensation of fullness or pain in the ear).
- Accumulation of cerumen as a cause of hearing loss is especially
significant in the elderly population.
- It attempts to clear the external auditory canal with matches, hairpins, and
other implements are dangerous because trauma to the skin, infection, and
damage to the tympanic membrane can occur.

Clinical Manifestation:
• otalgia ( sensation of fullness or pain in the ear)
• hearing loss
• vertigo
• fever

Assessment and Diagnostic findings:

• Cerumen can be removed by Irrigation, Suction, and Instrumentation
Unless the patient has perforated eardrum or an inflamed external ear.
• Gentle Irrigation usually helps remove impacted cerumen, particularly if it is
not tightly packed in the external auditory canal.
• For successful removal, the water stream must flow behind the obstructing
cerumen to move it first laterally and then out of the canal.
• To prevent injury, the lowest effective pressure should be used, however,
If the eardrum behind the impaction is perforated, water can enter the middle
ear, producing acute vertigo and infection.
• If irrigation is unsuccessful, direct visual, mechanical removal can be
performed on a cooperative patient trained by health care provider.
• If the cerumen cannot be dislodged by these methods, instruments such as a
cerumen curette, aural suction, and a binocular microscope for magnification
can be used.

Medical Management:
• Ceruminolytic agents such as peroxide in glyceryl(Deborox).
• Instilling a few drops of warmed glycerin, mineral oil, or half strength
hydrogen peroxide into the ear canal for 30 minutes can soften cerumen
before its removal.
 • Using any softening solution two or three times a day for several days is
generally sufficient

FOREIGN BODIES

- Some objects are inserted intentionally into the ear by adults who may
have been trying to clean the external canal or relieve itching or by
children who introduce peas, beans, pebbles, toys, beads and insects
may also enter into the ear canal.

Clinical Manifestation:
• Conductive hearing loss
• otalgia
• vertigo
• dizziness
• swelling

Assessment and Diagnostic findings:

• The three standard methods for removing foreign bodies are the
same as those for removing cerumen: Irrigation, suction, and
instrumentation.
• Foreign vegetable bodies and insects tend to swell; thus
irrigation is contraindicated.

Medical Management:
• Instilling mineral oil can kill the insects and allow it to be
removed.
• Attempts to remove a foreign body from external canal may be
dangerous in unskilled hands.
• The object may be pushed completely into the bony portion of
the canal, lacerating the skin and perforating the tympanic
membrane.
• In some circumstances , the foreign body may have to be
extracted in the operating room with the patient under general
anesthesia.
 EXTERNAL OTITIS (OTITIS EXTERNA)

- it refers to an inflammation of the external auditory canal.

Pathophysiology:
• External Otitis causes include water in the ear canal(swimmer’s ear)
• Trauma to the skin of the ear canal, permitting entrance of
organisms into the tissues and systemic conditions such as vitamin
deficiency and endocrine disorders.
• The most common bacterial pathogens associated with external
otitis are Staphylococcus aureus and Pseudomonas.
• The most common fungus isolated in both normal and infected ears
is Aspergillus.
• External otitis is often caused by a dermatosis such as psoriasis,
eczema, or seborrheic dermatitis.

Clinical Manifestation:
• pain
• discharge from the external auditory canal
• aural tenderness.
• Fever
• Cellulites
• lymphadenopathy.
• pruritus
• hearing loss or feeling of fullness

Assessment and Diagnostic findings:

• An otoscopic examination, the ear canal is erythematous and
edematous.
• Even allergic reactions to hair spray, hair dye, and permanent wave
lotions can cause dermatitis, which clear when the offending agents
is removed.
• Discharge may be yellow or green and foul smelling.
• In fungal infections, hairlike black spores may even be visible.

Medical Management:
• Relieving the discomfort
• Reducing the swelling of the ear canal
• Eradicating the infection
• Patients may require analgesics for the first 48 to 92 hours.
 • Administer liquid medications such as Burow;s solution, and
Antibiotics such medications usually combined antibiotic and
corticosteroid agents.
• For cellulites or fever, systemic antibiotics may be prescribed.
• For fungal disorders, anti-fungal agents are prescribed.

Nursing Interventions:
• Nurses should instruct the patient not to clean the external auditory
canal with cotton-tipped applicators and to avoid events that
traumatize the external canal such as scratching the canal with the
fingernail or other objects.
• Trauma may lead to the infection of the canal.
• Patients should also avoid getting the canal wet when swimming or
shampooing the hair.
• Infection can be prevented by using antiseptic otic preparations after
swimming,(eg. swim ear, ear dry).
 MALIGNANT EXTERNAL OTITIS

- A more serious, rare, external ear infection (temporal bone osteomyelitis).

Pathophysiology:
• This Malignant external otitis is a progressive, debilitating, and
occasionally fatal infection of the external auditory canal, the
surrounding tissue, and the base of the skull.
• Pseudomonas aeruginosa is usually the infecting organism in
patients with low resistance to infection.(eg. patients with diabetes)

Clinical Manifestation:
• fever
• tinnitus
• vertigo
• pain
• loss of hearing

Medical Management:
• Standard parenteral antibiotic treatment includes the combination of
antipseudomonal treatment and an aminoglycosides both of which
have serious side effects, because aminoglycosides are nephrotoxic
and ototoxic, serum aminoglycosides levels and renal and auditory
function must be monitored during therapy.
• Successful treatment includes control of the diabetes, administration
of antibiotics(usually intravenously)
• Local wound care includes limited debridement of the infected
tissue, including bone and cartilage, depending on the extent of the
infection.

Nursing Interventions:
• Relieving pain
• Provide comfort
• Assess the patient
• Nurses and other health care practitioner must work with patients
who are hearing impaired and their families to identify practical and
effective means of communication.
• Nurses can serve as catalysts throughout the health care system to
ensure that accommodations are made to meet the communication
needs of the patients.
Masses of the External Ear

Exostoses are small, hard, bony protrusions found in the lower posterior bony portion
of the ear canal; they usually occur bilaterally.
Caused by an exposure to cold water, as in scuba diving or surfing
Most common are basal cell carcinomas on the pinna and squamous cell carcinomas in
the ear canal.

Gapping Earring Puncture

Gapping earring puncture results from wearing heavy pierced earrings for a long time
Or after an infection, or as a reaction from the earring or other impurities in the
Earring.
The edges of the perforations are excised on the lateral and medial surfaces of the
earlobe
Next, the entire tract is removed, joining the above two incisions and resulting in a
much larger defect that is closed separately on each surface.
Then an antibiotic dressing is applied.
 CONDITIONS OF THE MIDDLE EAR

Tympanic Membrane Perforation

Perforation of the tympanic membrane is usually caused by infection or trauma.

Sources of trauma include skull fracture, explosive injury or a severe blow to ear.
Perforation is caused by foreign objects that have been pushed too far into external
auditory canal.
Injury to the ossicles and even the inner ear may result from this type of action.

Medical Management:

 In the case of a head injury or temporal bone fracture, a patient us observed for
evidence of cerebro spinal fluid otorrhea or rhinorrhea a clear watery drainage
from the ear or nose.
 While healing, the ear must be protected from water.

Acute Otitis Media

Acute otitis media is an acute infection of the middle ear, usually lasting less than 6
weeks.
The primary cause of acute otitis media is usually strep. Pneumoniae, H. influenzae
and Moraxella catarrhalis, which enters the middle ear after Eustachian tube
dysfunction caused by obstruction related to upper respiratory infections,
inflammation of surrounding structures, or allergic reactions.

Clinical Manifestations:

 Otalgia
 Drainage from the ear, fever and hearing loss
 The tympanic membrane is erythematous and often bulging.

Medical Management:

 Appropriate broad-spectrum antibiotic therapy

 Antibiotic otic preparation