ragay - notes of eent

8/9/2019 Ragay - Notes of Eent

1/15

Care of Clients with Disorder of Special Senses

Eyes

Assessment of Vision

Color vision Ishihara chart Peripheral vision - Confrontational test Extraocular muscle function Six cardinal gaze Visual acuity Snellens chart

- 20/40 client can see what a normal person can see in 40 ft Opthalmoscopy -examines internal and external structure of eye

- red reflex -reflection of light on vascular retina, absent means opacity of lens

- Also assess pupils and sclera

Diagnostic Tests

Fluorescein angiography

Imaging of ocular circulation with the use of fluorescein dye Pre procedure: check allergies, mydriatics 1 hr before the test Post procedure: skin may be yellow, increase fluids, urine may appear bright green

Computed tomography

Slit lamp Examination of anterior ocular structures under microscopic magnification

Corneal staining

Topical dye is instilled into conjunctival sac to outline irregularities in corneal surface -ask client to blink after application to distribute the dye -viewed in blue filter, bright green indicates non intact corneal epithelium

Tonometry

Assess intraocular pressure ( 10 - 21 mmHg)Snellens Chart Ishihara Plate Tonometer

Otoscope and Opthalmoscope Slit Lamp


2/15

Inflammatory Lid Infections

1. Blepharitis

Inflammatory reaction of the eyelid margin caused by bacteria(S. aureus), seborrheic skin conditionClinical Manifestations

foreign body sensation in the eye burning eye sensation Excessive tearing Itching Light sensitivity ( photophobia ) Red eyelids Crusting of the eyelashes ( scaling of eyelids) Matted eyelashes Loss of eyelashes

Complications

Stye Chalazion Conjunctivitis Trichiasis

Diagnostics

1. Culture and Sensitivity Test 2. Lid Biopsy

Nursing Management

1. Lid hygiene clean and free of exudates2. Scrub eyelid margin once daily ( soap/shampoo)3. Teach pt. method for applying warm compress4. Antibiotic opthalmic ointment applied after 15 minute application of warm compresses5. Explain the need for antibiotic regimen compliance

2. Chalazion

A.k.a. --- Meibomian gland lipogranuloma ( cyst / mass in the eyelid ) Cause : inflammation of a blocked meibomian gland ( usually upperlid )

Pathophysiology

1. Blocked meibomian gland

2. Accumulation of oil within the gland till it forms a lump in the eyelid

3. Eventually, the gland ruptures and releases the oil into the tissue of the eyelid

4. Inflammatory s/sx more painful and larger compared to styes

3. Styes ( Hordeulom )

Red, painful lump on the edge or inside of the eyelid that may look like a boil or a pimple.Clinical Manifestations

Pain Eyelid Swelling Light sensitivity Scratchy eye sensation Tear Usually filled with pus


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Risk Factors

Poor hygiene habits contact lens not clean before using Using expired cosmetics Leaving eye make up on overnight

Predisposing Factors

Chronic blepharitis ( bacterial infection caused by Staplyloccocus)Management

Application of topical antibiotic cream I & D procedures for pus- filled styes that wont rupture or burst on their own done by opthalmologist relieve pain

and pressure No need for oral antibiotics unless there is a generalized infection

Nursing Care

1. Warm compress application for 10 mins. QID2. Hand washing3. Take care with cosmetics4. Contact lenses should be clean

4. Conjunctivitis - Pink Eye

Inflammation of the conjunctivaCauses :

viruses bacteria ( gonorrhea or chlamydia ) Irritants(shampoos, dirt, smoke, pool chlorine) Allergies ( dust, pollens, contact lens allergy )

Manifestations

Redness in the white of the eye or inner eyelid Increased tearing Thick yellow discharge that crusts over eyelashes Itchy eyes Burning eye sensation Blurred vision Increased sensitivity to light

Management

Antibiotics ( tid/qid for 3-4 days) Eye drops Use water to wash the eye for conjunctivitis caused by irritating substances

Health Teachings

Dont rub or touch infected eye Hand washing/Proper hygiene Wash any discharge from the eye (b.i.d) using cotton ball/towel Wash contaminated bed linens, pillow cases Dont share make up Never wear another persons contact lenses Wear eye glasses instead of contact lenses Avoid sharing common articles (towels/glasses) Dont use eye drops in a non-infected eye that were used for an infected one

5. Keratitis - Any inflammation of the cornea

Pathophysiology

1. PF : trauma, URTI, Rheumatic Heart Fever

2. disintegration of corneal epithelium

3. Stromal layer becomes excellent culture medium for organisms( bacteria, fungi, virus )

4. Inflammation of the cornea

5. Irritation of the cornea

6. S/sx - severe pain, increased tearing,

photophobia, blurred vision

Management

Antibiotic eyedrops Systemic antibiotics


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CycloplegicsComplications

1. Blindness

Congenital Eye Problems

Refractive Errors individual differences in the formation & growth of the eyeball & cornea frequently result in

inappropriate

focal image formation

Emmetropia

Normal vision light rays are bent or refracted to be properly focused in the retinaMyopia

NearsightednessHyperopia

FarsightednessAstigmatism

Irregular or abnormal curvature of cornea or lens inability of the optics of the eye to focus a point object into a sharp focused image on the retina

Myopia A.k.a Nearsightedness

Light rays are entering the eye parallel to the optic axis arc are brought to a focus in front of the retina. Results from overly curved cornea or from the eyeball being too long from front to back Etiology : unknown, hereditary

Hereditary------------------ Genetic pathogenesis

Overly curved cornea-----thick cornea, thick lens

axial lengthening

axial length longer than the focal point of the refraction

* Light or visual image is focused in front of the retina manifestations : blurred vision of distant objects, headache, squints

to view far away objects

Hyperopia.. A.k.a Farsightedness

Rays of light entering the eye parallel to the optic axis are brought to a focus behind the retina Results from the eyeball being too short from front to back

PF : heredo -------------- familial

eyeball is too short Focusing power : too weak

weakens lenscx: strabismus

* Visual image or light is focused behindthe retina

Manifestations : aching eyes, blurred vision for

close objects, headache

Nursing Management for refractive disorders

Let patient wear corrective glasses/contact lenses Caution patient that wearing contact lenses can cause complications (corneal ulcer, abrasions) Eyeglasses: easy to use, durable, available and low cost. Contact lenses: hard/soft lens


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STRABISMUS

-is caused by a lack of coordination between the eyes. As a result, the eyes look in different directions and do not focusat the same time on a single point.

PATHOPHYSIOLOGY:

A. Paralytic (unknown, congenital, injuries to the orbit of the eye, diabetes, CVA)

1. loss of circulation to the eye 2. weakness of CN supplying EOM (3,4,6) 3. weakness or paralysis of one or more EOM 4. affected eye fixates 5. unaffected eye in a secondary deviated position 6. affected eye requires an excess of innervated impulse to maintain fixation 7. excess impulse are distributed to the unaffected eye 8. overaction ofEOM

B. Non paralytic (uncorrected hyperopia)

1. persistent deviation of gaze 2. overaction or underaction of the muscles in some fields of gaze

Manifestations:

1. eyes appear crossed 2. eyes do not align in some direction 3. uncoordinated eye movement 4. double vision

Management:

non-surgical treatment includes patching, pleoptics & prism glassesBLINDNESS

BCVA of20/400 to no light perception.LEGAL BLINDNESS

Is a condition of impaired vision with a BCVA that does not exceed 20/200 in the better eye or whose widest visualfield diameter is 20 degrees or less

Nursing Management for Blindness

1. Promoting coping efforts

2. Promoting spatial orientation & mobility

Train patient using auditory & tactile cues by providing anticipatory information Train patients mobility by using long cane, electronic travel aids, dog guides, orientation aids. Sighted guide technique-sighted person to assist3. Teaching Patients self-care

ASTIGMATISM

unequal curvature on the refractive surfaces of the eye.P.F: unknown, could be present at birth

Occurs with myopia & hyperopia

Non-spherical corneal surface

Unequal curvature of the eyes refractive surfaces

Light is spread over a more or less diffuse area

Difficulty seeing fine details either near or far

EYE CONTUSION

-is an injury to the eye that does not break the superficial layer, caused by a blow and characterized by swelling, discoloration

and pain.

Pathophysiology

A. Blunt traumatic injuries

1. Mechanical force against eye structure 2. Increase pressure or rapid decompression 3. Retinal detachment, Intraocular tissue, avulsion herniation


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Management

1. Eyeglasses2. Contact lenses

a. soft contact lenses larger but better tolerated, resemble thickness of plastic

wrap and can be worn for longer periods

b. hard lenses correct refractive errors by changing the shape of the cornea, increasing refractive ability

Surgical Management

1. Radial Keratotomy 8 to 16 diagonal incisions are made through 90% of the peripheral cornea. Central cornea is notincised.

Vision is not diminished. Flattens the cornea, decreases the length of the eye, image is more focused closer to the retina.

2. Epikeratophakia donor corneal tissue is surgically grafted into the clients own cornea to alter its refractive ability.

3. Photorefractive Keratectomy

Out-patient procedure under local anesthesia

- involves laser application of a powerful beam of ultraviolet light on the central cornea.

-Beam removes small portions of the tissueSurface, reshaping the cornea to properly focus an image on the retina

B. Penetrating injuries

1. Eye wall, corneal, scleral rupture 2. Conjunctival laceration 3. damage of anterior chamber angle -- tearing of the vessels of the iris 4. shallow anterior chamber hyphema (hemorrhage within the chamber 5. hemorrhagic chemosis (edema of the conjunctiva) 6. marked loss of vision -- ruptured globeManagement:

The goals of treatment are prevention of rebleeding and prolonged increase in IOP Moderate activity restriction Application of eye shield - Application of eye shield, e.g. stiff paper cup shield innovative substitute when

metal shield is unavailable

Meds:

-Topical corticosteroids reduce inflammation

-Anti-fibrinolytic agents - stabilize clot formation at the site of hemorrhage

-Aspirin is contraindicated

Surgery:

Vitrectomy-for traumatic retinal detachmentsPrimary enucleation (complete removal of the eyeball & part of the optic nerve)-done if globe is irreparable and has

No light perception

Complication:

Sympathetic opthalmia - an inflammatory condition created in the fellow eye by the affected eye; it may result inblindness of the fellow eye

OCULAR BURNS

-an injury to ocular tissues caused by heat, chemicals, radiation or gases in which the extent of the injury is determinedby the amount of exposure to the cell to the agent and to the nature of the agent.

Pathophysiology

A. ALKALI BURNS (lye, ammonia)

Penetrate the ocular tissues rapidly Immediate rise in IOP Keratopathy (spotty damage to the cornea) Subconjunctival hemorrhage Tissue ulceration

B. ACIDS (bleach, refrigerant)

1. Damage to the ocular tissue 2. Formation of precipitated Necrotic Tissue

Proteins - (acts as a barrier from further penetration and damage)

3. Keratopathy (spotty damage to the cornea) 4. Subconjunctival hemorrhage 5. Tissue ulceration


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C. THERMAL INJURY (iron, ash)

1. Burn on the eyelids

2. Blepharospasm (spasm of the eyelid muscles that result in closure of the lids)

3. Tissue ulcerationD. PHOTOCHEMICAL INJURY (ultraviolet injury, sun gazing)

corneal epithelial defect (tissue ulceration) corneal opacity conjunctival chemosis congestion of blood vessels The goal is to prevent tissue ulceration and promote re-epithelialization. Tap water irrigation of the corneal surfaces, conjunctival fornices. Local anesthesia by anesthesiologist/surgeon treat blepharospasm Remove particulate matter by using moistened, cotton-tip applicators Irrigation continues until conjunctival ph normalizes (7.3 -7.6) Intense lubrication using nonpreserved tearsMeds: AntibioticTherapy

Surgery:

Oculoplastic surgery - scarring of the eyelids Corneal surgery - corneal scarring

GLAUCOMA

Increased IOP due to inadequate drainage of aqueous humor from the canal of Schlemm or overproduction of aqueoushumor

Acute / Close/ Narrow Angle Glaucoma

Results from obstruction of outflow of aqueous humorChronic / Open / Wide Angle Glaucoma

Results from overproduction or obstruction of outflow of aqueous humorRisk Factors:

Ocular Hypertension, old age, African-American descent, myopia, previous history of glaucoma, steroid use, severediabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession

glaucoma); and uveitis (uveitic glaucoma).

Pathophysiology

Mechanical blockage of anterior chamber: results in accumulation of aqueous humor Pupillary dilation or forward displacement of the iris Angle closure occurs Scar tissue forms within the iris and cornea closing the angle Atrophy of the iris and ciliary body and optic nerve and degeneration of cornea because of edema

Assessment

Elevated IOP Loss of peripheral vision Difficulty adjusting the eye in low lighting Photophobia Blurred vision Halos around light Eye pain Frontal headache

Diagnostic Evaluation

Tonometry -elevated IOP, usually greater than 50 mmHg. Ocular examination may reveal a pale optic disk. Gonioscopy (using an instrument called a gonioscope) to study the angle of the anterior chamber of the eye.

Medical Management:

Emergency Pharmacotherapy is initiated to decrease eye pressure before surgery. Parasympathetic drugs used as miotic drugs -pupil contracts; iris is drawn from cornea; aqueous humor may

drain through lymph spaces (meshwork) into canal of Schlemm.

Carbonic anhydrase inhibitor -restricts action of enzyme that is necessary to produce aqueous humor. Beta-blockers -nonselective-may reduce production of aqueous humor or may facilitate outflow of aqueous

humor.

Hyper osmotic agents -to reduce intraocular pressure by promoting diuresis.


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Surgical Management: Indicated if:

-IOP is not maintained within normal limits by medical regimen.

-There is progressive visual field loss with optic nerve damage.

Peripheral iridectomy - excision of a small portion of the iris whereby aqueous humor can bypass pupil. Trabeculectomy - partial-thickness sclera resection with small part of trabecular meshwork removed and

iridectomy.

Laser iridotomy - multiple tiny laser incisions to iris. Other eye is usually operated as a preventive measure.Complications:

Uncontrolled intraocular pressure that can lead to optic atrophy and total blindnessNursing Interventions:Relieving pain:

Administer narcotics and other medications as directed. Medications that may produce nausea andvomiting are avoided. Patient may be medicated with antiemetic if nausea occurs.

Explain to patient that the goal of treatment is to reduce IOP as quickly as possible. Explain the procedures to the patient. Reassure patient that, with reduction in IOP, pain

Relieving Fear

Provide reassurance and calm presence to reduce anxiety and fear. Prepare patient for surgery if necessary. Describe procedures to patient. Patch will be worn for several hours, and sunglasses may help with photophobia Vision will be blurred for the 1st few days after the procedure Frequent initial follow up will be necessary to ensure control of IOP.

Management for Glaucoma

Osmotic diuretic Peripheral iridectomy Miotics B-Blockers Adrenergic agonist Carbonic anhydrase inhibitor Trabeculoplasty

Acute: medical emergency

-osmotic diuretic: IV diamox reduces the formation of aqueous humor

-Peripheral iridectomy allows aqueous humor to flow

Chronic

-B-Blockers, Adrenergic agonist, Carbonic anhydrase inhibitor decrease production of aqueous humor

-lifelong medication

-trabeculoplasty creates opening for aqueous humor to flow to conjunctival space

CATARACT

Opacity of the lens that distorts image projected onto the retinaAssessment

Painless blurring of vision Opaque or cloudy white pupil Absence of red reflex Vision that is better with dim light Photophobia

RETINAL DETACHMENT

Separation of layers of retinaTypes

Rhegmatogenous

Accumulation of fluid between layersTraction

Due to tension or pulling forceExudative

Due to production of serous fluid under the retina


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Assessment

Sense of curtain being drawn Flashes of lights Floaters Loss of portion of visual field Painless

Immediate management

-Bed rest

-patch both eyes-affected side down

Surgical procedures

Vitrectomy Drain fluid Cryosurgery Seals retinal breaks Diathermy stimulates inflammatory process Laser therapy stimulates inflammatory response Scleral buckling hold choroid and sclera together Insertion of gas or silicone oil

-(Diathermy uses electrode needle and heat)

-Inflammatory response seals the tear

-Insertion of gas or silicone oil- float against retina. Affected side down.

Postop care

-bed rest 1-2 days

-no reading for 3-5 weeks

-monitor for IOP

-Eye patch at night

-area affected should be in upper position

MACULAR DEGENERATION

loss of vision in the center of the visual field (the macula) because of damage to the retina Occurs mostly with people above 60 y.o Laser treatment Use of bright lights and magnification device Amsler Grids to detect loss of vision

The Amsler Grid consists of evenly spaced horizontal and vertical lines printed on black or white paper. A small dot is located in

the center of the grid for fixation. While staring at the dot, the patient looks for wavy lines and missing areas of the grid.

Eye Injuries

Hyphema

Blood in the anterior chamber d/t trauma Resolves in 5-7 days

Contusion

Bleeding into the soft tissue d/t trauma Causes black eye

Penetrating objects

Do not remove object Cover object with a cup Cover both eyes

Chemical burns

Flush eyes for 15-20 mins


10/15

EARS

Assessment

1.Otoscopic Examination

Used to examine auditory canal and tympanic membrane2. Tuning Fork Test

Weber

Rinne

3. Romberg's test

Diagnostic

Audiometry - Measures Hearing acuity

Inflammatory Conditions : EarOTITIS MEDIA

a chronic inflammation of the middle ear with tissue damage. It may be caused by an antibiotic-resistant organism or a particularly virulent strain of organism. ETIOLOGY : repeated episodes of ACM, Risk Factors : Chronic systemic disease ,immunosuppressionPATHOPHYSIOLOGY :

1. Repeated episodes of ACM

2. accumulation of inflammatory exudates in the middle ear cavity may result in necrosis of tissue, with damage to the

tympanic membrane & possibly the ossicles.

3. Persistent rupture of the tympanic membrane and damage to the ossicles

4. Interrupted transmission of sound

5. Conductive hearing lossmastoiditis, cholesteatoma

CLINICAL MANIFESTATIONS

Painless or dull ache and tenderness of mastoid. Otorrhea (odorless or foul smelling) Vertigo and pain ( present if with CNS complications possible rupture of tympanic membrane. F

ever and postauricular erythema & edema.DIAGNOSTIC EVALUATION

Audiometric tests ( Air conductive hearing loss is present ) X-rays ( note mastoid pathology, for example, cholesteatoma or haziness of mastoid cells ). Culture of exudates from middle ear

Medical Therapy

Antibiotic and steroid eardrops IV antibiotics must cover beta-lactase-producing organisms-ampicillin-sulbactam (Unasyn), cefuroxime (Ceftin).

Surgical Interventions

Types of procedures:

Simple mastoidectomy- removal of diseased bone and insertion of a drain Radical mastoidectomy- removal of posterior wall of ear canal, remnants of the tympanic membrane, the

malleous & incus.

Posteroanterior mastoidectomy - simple mastoidectomy + tympanoplasty Antibiotic and steroid eardrops may control middle ear infection and inflammation, but once

mastoiditis develops, parenteral antibiotic therapy is necessary.

Ear drops containing neomycin, garamycin, tobramycin, and quinolones such as Ciprofoxacin (cipro) areinstilled into the middle ear when the tympanic membrane is ruptured.

Surgical Interventions Indicated when cholesteatoma is present. Indicated when there is pain, profound deafness, dizziness, sudden facial paralysis, or stiff neck (may

lead to meningitis or brain abscess).

Simple mastoidectomy-; indicated when there is persistent infection and signs of intracranialcomplications.

tympanoplasty (reconstruction of middle ear structures).


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COMPLICATIONS

Acute and chronic mastoiditis Cholesteatoma CNS infection (meningitis, intracranial abscess) Postoperatively-facial nerve paralysis, bleeding, vertigo

NURSING ASSESSMENT

Assess for history of ear infection and treatment compliance. Assess for ear drainage, patency of tympanic membrane Assess for hearing loss Palpitate for mastoid tenderness

PATIENT EDUCATION & HEALTH MAINTENANCE

Teach patient to keep ear dry-avoid showers, washing hair, swimming-to prevent any water from gaining access tomiddle ear.

Encourage patient to follow up for frequent ear cleaning. Stress the importance of adhering to antibiotic schedule Advise of complications and to report headache, change in mental status or arousal, or increased ear pain. Stress the importance of follow-up hearing evaluations and early intervention for any signs of ear infection in the

future.

LABYRINTHITIS

an inflammation of the inner ear vestibular labyrinth system. The hallmark is vertigo.ETIOLOGY :

1. viral or bacterial infection2. occur as a symptom of a tumor or other pathology in the nervous system3. occur due to a physiologic response from external stimuli.

PATHOPHYSIOLOGY

1.URTI virus, mumps, rubella, rubeolla, and influenza, bacterial meningitis, complication, otitis media & cholesteatoma,

various stimuli (roller coaster ride, sudden stop, quick change in position )

2. Results to conflicting vestibular, somato- sensory signals

3. Sudden on set of incapacitating vertigo, nausea, and vomiting, hearing loss and tinnitus

4. Symptoms may remain steady or gradually increase with CNS pathology

DIAGNOSTIC EVALUATION

ENG with caloric and dolls eye testing to differentiate cause. CT or MRI for suspected tumors of cranial nerve VIII

MANAGEMENT Antibiotics Viral and physiologic causes are treated with symptomatic support. Prevention and management of attacks. Vestibular suppressant and antiemetic medication Presumed pathologic causes are worked up, cause is treated with neurosurgery

Characteristic infectious labyrinthitis may be Monitored for improvement without diagnostic testing. bacterial labyrinthitis are treated with antibiotics antiemetic medication (meclizine, diazepam, promethazine).

COMPLICATIONS

Permanent hearing loss Injury from fall

NURSING ASSESSMENT

Assess frequency and severity of attacks and how patient handles them. Assess for fever related to bacterial infection. Assess for additional neurologic symptomsvisual changes, change in mental status, sensory and motor deficits, -

indicate CNS pathology

Assess for effectiveness of vestibular stimulants and antiemetics. If fall occurs, assess for injury.

NURSING DIAGNOSIS

High Risk for Injury related to gait disturbance secondary to vertigo Anxiety related to sudden onset of symptoms


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Risk for Fluid Volume Deficit related to vomiting and Impaired intake Self-Care Deficit (bathing, dressing, feeding, toileting) related to vertigo

NURSING INTERVENTIONS:

Preventing Injury

At onset of attack, have patient lie still in darkened room with eyes closed or fixed on stationary object, until thevertigo passes.

Ensure that patient can obtain help at all times through use of call system, close proximity to staff, or companion. Remove any obstacles in patients environment. Ensure that sensory aids are availableglasses, hearing aid, proper lighting. Use side rails while patient is in bed.

Administer medications as directed; assess for and avoid oversedation.MINIMIZING ANXIETY

Explain the physiology behind vertigo & possible triggers. Support patient and family through the diagnostic process. Assist patient to adjust activities to minimize the impact. Teach stress reduction techniques

ENSURING ADEQUATE FLUID

Keep diet light while vertigo is present. Administer antiemetics as directed. Assess intake and output as indicated. Encourage fluids and small feedings while patient is feeling better.

ENCOURAGING SELF-CARE

Encourage activity while vertigo is minimal; rest during attacks. Set up environment for patients safety and Assist patient with hygiene and other care as needed.

PATIENT EDUCATION & HEALTHMAINTENANCE

Teach safety measures during vertigo attacks. Tell patient that vertigo is best tolerated while lying flat in bed in a darkened room with eyes closed or looking at

stable object.

Teach patients how to take medications, and to avoid other CNS depressants such as alcohol. Encourage follow-up.

MENIERES DISEASE

endolymphatic hydrops - a chronic disease that involves the inner ear and causes a triad of symptomsvertigo, hearingloss, and tinnitus.

Etiology : exact cause unknownIncidence :

Usually unilateral, later may become bilateral. Occurs most frequently between age 30 and 60. Severity of attacks may diminish over the years, but hearing loss increases

PATHOPHYSIOLOGY :

1. PF : middle ear infection, head trauma ,URTI or by using aspirin, smoking cigarettes or drinking alcohol, narrowed

endolymphatic duct, too much fluid secreted by stria vascularis

2. Swelling of the endolymphatic sac & other tissues in the vestibular system of the inner ear

3. Endolymphatic fluid bursts from its normal channels in the ear and flows into other areas causing damage

4. HYDROPS form5. Fluid distention of the endolymphatic spaces of the labyrinth destroys cochlear hair cells

CLINICAL MANIFESTATIONS

Vertigo ( 10 mins. to several hours ) Dizziness, tinnitus, reduced hearing-involved side. Headache, nausea, vomiting & incoordination Irritability;other personality changes. Tinnitus and impaired hearing

DIAGNOSTIC EVALUATION

Caloric test/ENG Fluid, above or below body temperature, is instilled into the auditory canal. Will precipitate an attack in patients withMenieres disease.

Audiogram shows sensorineural hearing loss. CT, MRI to rule out acoustic neuroma.

Sudden attacks occur, in which patient feels that the room is spinning (vertigo); may last 10 minutes


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to several hours. History often reveals ear trouble, vasomotor rhinitis, and allergies. Caloric test/ENG to differentiate Menieres disease from intracranial lesion. Will precipitate an attack in patients withMenieres disease. Normal patient complains of dizziness; patient with acoustic neuroma has no reaction.

MEDICAL MANAGEMENT

Administration of the vestibular suppressant to control symptoms.

Meclizine (Antivert,Bonine) up to 25 mg qid Diphenhydramine (Benadryl) 25 to 50 mg tid to qid Diazepam (Valium) 2 mg tid or 5 to 10 mg IM or IV (addictive potential)

Streptomycin (IM) or gentamycin (transtympanic injection) may be given to selectively destroy vestibular apparatus (if vertigo is uncontrollable)

Additional antiemetic such as promethazine (Phenergan) (may be needed to reduce nausea, vomiting and resistantvertigo).

Surgical Management

Conservative - simple endolymphatic sac decompression or endolymphatic subarachnoid or mastoid shunt Destructive surgery

Labyrinthectomy - results in total deafness of affected ear. Vestibular nerve section-neurosurgical suboccipital approach to the cerebellopontine angle for intracranial

vestibular nerve neurectomy.

Conservative- simple endolymphatic sac decompression or endolymphatic subarachnoid ormastoid shunt to relieve symptoms without destroying function.

Destructive surgery; Labyrinthectomy-recommended if the patient experiences progressive hearing loss and severe

vertigo attacks so normal tasks cannot be performed; results in total deafness of affected ear.

Vestibular nerve section-neurosurgical suboccipital approach to the cerebellopontine angle forintracranial vestibular nerve neurectomy.

NURSING INTERVENTIONS

A.Ensuring Safety

Help patient recognize aura so patient has time to prepare for an attack. Encourage patient to lie down during attack, in safe place and lie still. Put side rails up on bed if in hospital. Have patient close eyes if this lessens symptoms. Inform patient that the dizziness may last for varying lengths of time.

B. MINIMIZING FEELINGS OF ISOLATION

Provide encouragement and understanding. Assist patient to identify specific triggers to control attacks. Remind the patient to move slowly Avoid noises and glaring, bright lights Control environmental factors and personal habits If there is a tendency to allergic reactions to foods, eliminate those foods from the diet.

OTOSCLEROSIS

s a pathologic condition in which there is formation of new spongy bone in the labyrinth, fixation of the stapes, andprevention of sound transmission through the ossicles to the inner fluids, resulting in deafness.

ETIOLOGY : unknown, BUT there is a familial tendency, more women affected than men. Congenital / autosomal patterns.PATHOPHYSIOLOGY :

1.begins with resorption of bone in one or more foci

2. Bone appears spongy than normal

3. Resorbed bone then replaced by an overgrowth of new, sclerotic bone4. Process is slowly progressive, invading more areas of the temporal bone, ( stapes of the footplate)5. Pathologic bone immobilizes the stapes

6. Reduced transmission of sound, pressure on inner structures, vestibulocochlear nerve

MANIFESTATIONS

Tinnitus, conductive / mixed hearing loss, vertigo Progressive loss of soft spoken tones


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Diagnostics :

1. Audiometry findings - substantiate conductive or mixed hearing loss.

2. Bone conduction is much better than air conduction.

MANAGEMENT

No known medical treatment exists for this form of deafness, but amplification with a hearing aid may be helpful.Surgery

stapedectomy. That removal of otosclerotic lesions at the footplate of stapes or complete removal of the stapes and the

creation of a tissue implant with prosthesis to maintain suitable conduction.

To perform such delicate surgery, the otologic binocular microscope is used.Hearing loss

Conductive

Sound waves are blocked to the inner ear fibers because of external or middle ear problem Can be caused by inflammation, tumor, otosclerosis

Sensorineural

Problems with the inner ear or sensory fibers that leads to the cerebral cortex Damage is permanent

Conductive/ sensorineural

PSYCHOGENIC HEARING LOSS- usually a manifestation of an emotional disturbance and unrelated to evident structural

changes in the hearing mechanisms. Loss is often total, but without physical basis, the patient may suddenly recover.

Presbycusis

Associated with aging d/t degeneration of ganglion cells in the cochlea and loss of elasticity of basilar membranes Gradual bilateral hearing loss Deafness in higher tone

Incidence : 65-75 YEARS OF AGE, 40% OF population older than 75 yrs. Old, men more than women

ETiology : Degenerative changes in the ear ( hair cells-organ of corti )

PATHOPHYSIOLOGY :

1. Old age ( 65-75 yrs. Old )

Pf : chronic noise exposure, vascular disorders

2. Degenerative changes ( loss of neuroepithelial hair cells, neurons, stria vascularis

3. (snhl) hearing loss results

Manifestations : Diff. In understanding words in a noisy environment Reports hearing soft whispered, normally spoken or shouted words Loss of high frequency sound descrimination first

MANAGEMENT :

All other possibly treatable hearing disorders should be ruled out before this diagnosis. There is no effective medicalor surgical treatment.

The patient should be counseled by an otologist (physician who specializes in the ear) in collaboration with anaudiologist (nonphysician provider who can suggest non-medical treatment).

Helpful aids should be considered, such as a telephone amplifier, radio and television earphone attachments, buzzersinstead of doorbell.

Understanding and help from family members are important.ACOUSTICNEUROMA

slow growing benign, tumor of CN VIII, arise from Schwann cells of vestibular portion of the nerveAssessment

unilateral tinnitus, hearing loss, with or without vertigo or balance disorderDiagnostic Exams

MRI CT scan

Management

surgery complications : facial nerve paralysis, CSF leak, meningitis, cerebral edema.


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Otitis Media

Infection of middle ear d/t blockage of eustachian tube A common complication of respiratory infection Fever, irritability and restlessness Otorrhea, purulent drainage and earache Pulling and rubbing of ear Antibiotic therapy Affected ear down Myringotomy

Myringotomy insertion of tympanoplasty tubes into the middle ear to equalize the pressure

-no tub bath

-ear plugs during bathing

-no blowing of nose

-no traveling by air

Otosclerosis

Bony overgrowth of the tissue surrounding the ossicles Progressive deafness especially at lower tone, bilateral conductive hearing loss (-) Rinne Test Webber test shows lateralization on the ear most affected Stapedectomy

ragay - notes of eent

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