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 examiner2. 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 sensorineuralhearing 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 managementAural 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 skills3. 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 ear2. Active drainage from the ear with in the previous 90 days

3. Sudden or rapidly progressive hearing loss with in the previous 90 days4. Complaints of dizziness or tinnitus5. Unilateral hearing loss that occurred suddenly or with in previous 90 days6. 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 surfingMost 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 earlobeNext, 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