DISEASES OF THE EYES

MACULAR DEGENERATION

(AGE-RELATED MACULAR DEGENERATION)

CLINICAL DESCRIPTION

Is a disease that destroys your sharp, central vision. You need central vision to see objects clearly and to do tasks such as reading and driving. AMD affects the macula, the part of the eye that allows you to see fine detail.

It does not hurt, but it causes cells in the macula to die. In some cases, AMD

advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision

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in both eyes. Regular comprehensive eye exams can detect macular degeneration before the disease causes vision loss. Treatment can slow vision loss.

It The disease is most common in people over age 60, which is why it is often called age-related macular degeneration.does not restore vision.

The retina is the inner layer of tissue at the back of the eye. It changes light and images that enter the eye into nerve signals that are sent to the brain. The macula is the part of the retina that makes vision sharper and more detailed.

ETIOLOGY

Damage to the area around blood vessels that supply the macula. This change in the blood vessels damages the macula. Scientists are not sure what causes AMD. The condition is rare before age 55, and is most often seen in adults 75 years or older.

In addition to heredity, other risk factors are:

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Caucasian raceCigarette smokingHigh-fat dietFemale genderObesity Two phases of macular degeneration (AMD) exist:Dry macular degeneration occurs when the blood vessels under the macula become thin and brittle. Small yellow deposits, called drusen, form. Almost all people with macular degeneration start with the dry form.

Wet macular degeneration occurs in only about 10% of people with macular degeneration. New abnormal and very fragile blood vessels grow under the macula. This is called choroidal neovascularization. These vessels leak blood and fluid. This form causes most of the vision loss associated with the condition.

SIGNS and SYMPTOMS

At first you may not have symptoms. As the disease progresses, your central vision may be affected.

The most common symptom in dry AMD:

Blurred vision. Often objects in the central vision look distorted and dim colors look faded

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You may have trouble reading print or seeing other details, but you can generally see well enough to walk and perform most routine activities.As the disease becomes worse, you may need more light to read or perform everyday tasks. Straight lines appear distorted and wavy. A blurred or dark spot in the center of vision gradually gets larger and darker.In the later stages, you may not be able to recognize faces until they are close.AMD typically does not affect side (peripheral) vision. This is very important, because it means complete vision loss never occurs from this disease.Central vision loss can occur very quickly. If this occurs, you will need urgent evaluation by an ophthalmologist with experience in retinal disease.

DIAGNOSTIC TEST

Fluorescein angiogram

This test helps the ophthalmologist find out more about your AMD and whether you have wet or dry AMD. Usually the network of blood vessels underneath your retina can't be seen by examining your eyes with a slit lamp. The ophthalmologist can see the damage to your retina but they can't see the detail of the blood vessels this way. A Fluorescein angiogram is a way of taking pictures of these blood vessels which allows the ophthalmologist to see if there are any changes which could be causing problems.

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Before a series of pictures is taken, a yellow dye is injected into your arm which then travels through your bloodstream to your eye. This usually isn't painful but can make some people feel sick. This dye makes the blood vessels visible on the pictures taken.

Once the dye has been injected you will be asked to look at a special machine. The machine takes pictures of the back of your eye as the dye is travelling through the blood vessels. You'll experience a series of flashing lights as the pictures are taken, but the test isn't painful. It usually takes about 10minutes.

It is a very common test and very few people have any serious side effects. The injection may give your skin a slight yellow tinge from the dye and it soon passes into your urine, which may also appear a darker yellow than normal (possibly for up to two to three days) but often it fades quicker than that. Some people are dazzled for a while after the flashing lights but most people find the test straightforward.

These tests help the ophthalmologist decide which type of AMD you have and if any treatment is possible.

MEDICAL MANAGEMENT

You will be given drops to enlarge (dilate) your pupils. The eye care provider will then use special lenses to view your retina, blood vessels, and optic nerve.

The doctor will look for specific changes in the macula and blood vessels. One of the earliest findings in dry AMD is drusen, the

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yellow deposits that form in the macula.

You may be asked to cover one eye and look at a pattern of lines called an Amsler grid. If the straight lines appear wavy, it may be a sign of AMD.

Other tests for macular degeneration may include:

Fluorescein angiogramFundus photographyOptical coherence tomography (OCT)

OTHER MEDICAL MANAGEMENT

A special combination of vitamins, antioxidants, and zinc may prevent the disease from getting worse if the macular degeneration is not yet severe. It will not bring vision that has been lost, however. This combination is often called the "AREDS" formula.

AREDS may also benefit people with a family history and risk factors for AMD before they have any signs of the disease.

Only take this vitamin combination if your doctor recommends it. Make sure your doctor knows about any other vitamins or supplements you are taking. Smokers should not use this treatment.

The recommended supplements contain:

500 milligrams of vitamin C400 international units of beta-carotene80 milligrams of zinc2 milligrams of copper

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Other supplements called lutein and zeaxanthin may also be helpful, although they are not part of the AREDS formula.Special medications that prevent new blood vessels from forming in the eye (anti-angiogenesis, anti-VEGF therapy) -- drugs such as bevacizumab (Avastin) and ranibizumab (Lucentis) are injected into the eye. This is a painless process.

SURGICAL MANAGEMENT

For wet AMD

Laser surgery (laser photocoagulation) -- a small beam of light destroys the leaking, abnormal blood vessels.Photodynamic therapy -- a light activates a drug that is injected into your body to destroy leaking blood vessels.Low-vision aids (such as special lenses) and therapy can help you use the vision that you have more effectively, and improve your quality of life.

For dry AMD

A complete eye exam should be performed by an eye specialist at least once a year.After getting treated for wet AMD, you will need frequent, perhaps monthly, follow-up visits.

In AMD, early detection of vision changes is very important. Early detection leads to earlier treatment and often, a better outcome.

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The best way to detect changes is by self-testing at home with an Amsler grid. Test each eye individually with the vision correction you normally wear for reading.

NURSING MANAGEMENT

Although there is no known way to prevent macular degeneration, lifestyle factors can reduce your risk of developing the condition:

Don't smokeEat a healthy diet that is high in fruits and vegetables and low in animal fatExercise regularly

Maintain a healthy weightSee your eye care professional regularly for dilated eye exams.

PAPILLEDEMA

DEFINITION

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Is optic disc swelling that is caused by increased intracranial pressure. The swelling is usually bilateral but can be unilateral which is extremely rare and can occur over a period of hours to weeks.

CLINICAL DESCRIPTION

In intracranial hypertension papilledema can occur in only one eye or it can be more severe in one eye than the other or may not occur at all despite evidence of raised intracranial pressure. When papilledema is present it is a pathological state and requires investigation to prevent loss of vision. Papilledema can often be a tell tale sign of intracranial hypertension. When there is papilledema in one eye one must also be sure that there is no local problem in the orbit (eye socket) that is causing unilateral papilledema. For example a tumor of the optic nerve behind the eyeball can also cause such swelling or blockage of circulation in the eye socket. It is important to have ultrasound and MRI studies to be sure.

ETIOLOGY

Raised intracranial pressure

Brain tumor

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Pseudotumor cerebri or cerebral venous sinus thrombosis, Intracerebral hemorrhageRespiratory failureHypotoniaAccutane (Isotretinoin), which is a powerful derivative of Vitamin A, rarely causes Papilledema.Hypervitaminosis A, in some people who take megadoses of nutritional supplements and vitamins.Hyperammonemia, elevated level of ammonia in blood (including cerebral edema/intracranial pressure)

Guillain-Barré syndrome due to elevated protein levelsFoster Kennedy syndrome (FKS)Chiari MalformationTumors of the frontal lobeAcute Mountain Sickness and High Altitude Cerebral OedemaLyme disease (Lyme meningitis specifically, when the bacterial infection is in the central nervous system, causing increased intracranial pressure).Malignant HypertensionMedulloblastoma

SIGNS and SYMPTOMS

Most symptoms in a patient with papilledema are secondary to the underlying elevation in intracranial pressure.

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Headache: Increased intracranial pressure headaches are characteristically worse on awakening, and they are exacerbated by coughing or other type of Valsalva maneuver.Nausea and vomiting: If the rise in intracranial pressure is severe, nausea and vomiting may occur. This eventually may be followed by a loss of consciousness, pupillary dilation, and death.Pulsatile tinnitus

Visual symptoms often are absent, but the following symptoms can occur:

Some patients experience transient visual obscurations (graying-out of their vision, usually both eyes, especially when rising from a lying or sitting position, or transient flickering as if rapidly toggling a light switch).Blurring of vision, constriction of the visual field, and decreased color perception may occur.

The signs of papilledema that are seen using an ophthalmoscope include

venous engorgement (usually the first signs)loss of venous pulsationhemorrhages over and / or adjacent to the optic discblurring of optic marginselevation of optic discPaton's lines = radial retinal lines cascading from the optic disc.

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DIAGNOSTIC TEST

Checking the eyes for signs of papilledema should be carried out whenever there is a clinical suspicion of raised intracranial pressure, and is recommended in newly onset headaches. This may be done by ophthalmoscopy or slit lamp examination.

PATHOPHYSIOLOGY

As the optic nerve sheath is continuous with the subarachnoid space of the brain (and is regarded as an extension of the central nervous system), increased pressure is transmitted through to the optic nerve. The brain itself is relatively spared from pathological consequences of high pressure. However, the anterior end of the optic nerve stops abruptly at the eye. Hence the pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve at its head. The fibers of the retinal ganglion cells of the optic disc become engorged and bulge anteriorly. Persistent and extensive optic nerve head swelling, or optic disc edema, can lead to loss of these fibers and permanent visual impairment.

MEDICAL MANAGEMENT

glucocorticoidsacetazolamide

SURGICAL MANAGEMENTPage | 12

Careful dilated fundus examination should be performed to look for the following signs:

Early manifestations

Disc hyperemiaSubtle edema of the nerve fiber layer can be identified with careful slit lamp biomicroscopy and direct ophthalmoscopy. This most often begins in the area of the nasal disc. A key finding occurs as the nerve fiber layer edema begins to obscure the fine peripapillary vessels.Small hemorrhages of the nerve fiber layer are detected most easily with the red-free (green) light.Spontaneous venous pulsations that are normally present in 80% of individuals may be obliterated when the intracranial pressure rises above 200 mm water. Therefore, though the presence of spontaneous venous pulsations is very useful to exclude papilledema (except in cases of highly variable intracranial pressure), its absence is not very helpful.

Late manifestations

As the papilledema continues to worsen, the nerve fiber layer swelling eventually obscures the normal disc margins and the disc becomes grossly elevated.Venous congestion develops, and peripapillary hemorrhages become more obvious, along with exudates and cotton-wool

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spots.The peripapillary sensory retina may develop concentric or, occasionally, radial folds known as Paton lines. Choroidal folds also may be seen.

Chronic manifestations

If the papilledema persists for months, the disc hyperemia slowly subsides, giving way to a gray or pale disc that loses its central cup.With time, the disc may develop small glistening crystalline deposits (disc pseudodrusen).

NURSING MANAGEMENT

The history should be taken, and a physical examination, including vital signs, should be performed. In particular, check the blood pressure to exclude malignant hypertension.The patient should be evaluated for neurologic problems and febrile illness.

CATARACT

CLINICAL DESCRIPTION

A cataract is a

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clouding that develops in the crystalline lens of the eye or in its envelope, varying in degree from slight to complete opacity and obstructing the passage of light. Early in the development of age-related cataract the power of the lens may be increased, causing near-sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially blinding if untreated. The condition usually affects both the eyes, but almost always one eye is affected earlier than the other

Age-related cataract is responsible for 48% of world blindness, which represents about 18 million people, according to the World Health Organization (WHO). In many countries surgical services are inadequate, and cataracts remain the leading cause of blindness. As populations age, the number of people with cataracts is growing. Cataracts are also an important cause of low vision in both developed and developing countries. Even where surgical services are available, low vision associated with cataracts may still be prevalent, as a result of long waits for operations and barriers to surgical uptake, such as cost, lack of information and transportation problems.

In the United States, age-related lenticular changes have been reported in 42% of those between the ages of 52 to 64, 60% of those between the ages 65 and 74, and 91% of those between the ages of 75 and 85.

The increase in ultraviolet radiation resulting from depletion of the ozone layer is expected to increase the incidence of cataracts.

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ETIOLOGY

Cataracts develop for a variety of reasons, including long-term exposure to ultraviolet light, exposure to radiation, secondary effects of diseases such as diabetes, hypertension and advanced age, or trauma (possibly much earlier); they are usually a result of denaturation of lens protein. Genetic factors are often a cause of congenital cataracts and positive family history may also play a role in predisposing someone to cataracts at an earlier age, a phenomenon of "anticipation" in pre-senile cataracts. Cataracts may also be produced by eye injury or physical trauma. A study among Icelandair pilots showed commercial airline pilots are three times more likely to develop cataracts than people with non-flying jobs. This is thought to be caused by excessive exposure to radiation coming from outer space. Cataracts are also unusually common in persons exposed to infrared radiation, such as glassblowers who suffer from "exfoliation syndrome". Exposure to microwave radiation can cause cataracts. Atopic or allergic conditions are also known to quicken the progression of cataracts, especially in children. Cataracts can also be caused by iodine deficiency.

Cataracts may be partial or complete, stationary or progressive, hard or soft.

Some drugs can induce cataract development, such as corticosteroids and Seroquel.

There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also classified by their

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location, e.g. posterior (classically due to steroid use) and anterior (common (senile) cataract related to ageing).

SIGNS and SYMPTOMS

As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted. Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare can be a problem as light is scattered by the cataract into the eye. The affected eye will have an absent red reflex. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is demonstrated an eye specialist consultation is recommended.

In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon appears to be confined to one eye only.

The symptoms of cataracts are very similar to the symptoms of ocular citrosis.

DIAGNOSTIC TEST

Decreased visual acuity is directly proportionate to cataract density. The SNELLEN VISUAL ACUITY TEST, OPTHALMOSCOPY, and SLIT-LAMP BIOMICROSCOPIC EXAMINATION are used to establish the degree of cataract formation. The degree of lens opacity does not always correlate with the patient’s functional status. Some patients

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can perform normal activities despite clinical significant cataracts. Others with less lens opacification have a disproportionate decrease in visual acuity; hence, visual acuity is an imperfect measure of visual imparment.

PATHOPHYSIOLOGY

Degeneration of lens into the cells

Increased water content in the cells

The entire lens become involved

Cellular debris from the lens escapes through thedegenerated lens capsule into the aqueous humor

The debris is phagocytized by macrophagesand contribute to the obstruction of

aqueous humor outflow

MEDICAL MANAGEMENT

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Aspirin should be withheld for 5-7 days, Nonsteroidal anti-inflammatory medications (NSAID’s) for 3 to 5 days, and warfarin (Coumadin) until the prothrombin time of 1.5 is almost reached when the patient undergo surgery to prevent the risk of retrobulbar hemorrhage.

SURGICAL MANAGEMENT

When a cataract is sufficiently developed to be removed by surgery, the most effective and common treatment is to make an incision (capsulotomy) into the capsule of the cloudy lens in order to surgically remove the lens. There are two types of eye surgery that can be used to remove cataracts: extra-capsular (extracapsular cataract extraction or ECCE) and intra-capsular (intracapsular cataract extraction, or ICCE).

Extra-capsular (ECCE) surgery consists of removing the lens but leaving the majority of the lens capsule intact. High frequency sound waves (phacoemulsification) are sometimes used to break up the lens before extraction.

Intra-capsular (ICCE) surgery involves removing the entire lens of the eye, including the lens capsule, but it is rarely performed in modern practice.

In either extra-capsular surgery or intra-capsular surgery, the cataractous lens is removed and replaced with a plastic lens (an intraocular lens implant) which stays in the eye permanently.

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Cataract operations are usually performed using a local anaesthetic and the patient is allowed to go home the same day.

NURSING MANAGEMENT

Antibiotic-steroids TobraDexAvoid heavy lifting, reading but watching tv is allowed, violent coughing, bending lower than waist.Prolonged anger and sexual activity.Wear glasses during the day until the pupils responds to light Eyeshield at night or while sleeping.Sleep on unoperated sideFor minor pain: use acetaminophen, ice or heat as prescribed.Shower or bathing is allowed.

Care of the dressings.Stool softenersNo aspirin due to clotting effects.

Instruct to report pain with nausea and vomiting.

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GLAUCOMA

DEFINITION and CLINICAL DESCRIPTION

Glaucoma is a disease where fluid pressure inside the eye increases causing irreversible damage to the optic nerve and loss of vision. It is

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often, but not always, associated with increased pressure of the fluid in the eye.

The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. There are many different sub-types of glaucoma but they can all be considered a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg or 2.8 kPa). One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.

Glaucoma has been nicknamed the "silent thief of sight" because the loss of vision normally occurs gradually over a long period of time and is often only recognized when the disease is quite advanced. Once lost, this damaged visual field cannot be recovered. Worldwide, it is the second leading cause of blindness. It is also the first leading cause of blindness among African Americans.Glaucoma affects 1 in 200 people aged fifty and younger, and 1 in 10 over the age of eighty. If the condition is detected early enough it is possible

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to arrest the development or slow the progression with medical and surgical means.

The word glaucoma comes from the opacity of the crystalline lens.

ETIOLOGY

Beta Blockers: Timolol-use caution to patient with Asthma and CHF.Miotics: Pilocarpine-constrict the pupil and increase contraction of the ciliary muscle causing increased outflow of Aqueous humor. S/E: can cause blurred vision and browache.SympathomimeticsMannitolCarbonic Anhydrase inhibitorEpinephrine: reduces aqueous humor output; drug of choice to patient with asthma and CHF.Acetazolamide: reduce aqueous production. S/E: nausea, malaise, numbness of extremities.

SIGNS and SYMPTOMS

Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. It is painless and does not have acute attacks. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).

DIAGNOSTIC TEST Page | 23

Direct OphthalmoscopyTonometry

Gonioscopy

PATHOPHYSIOLOGY

Normally, the aqueous humor, which is produced by the ciliary epithelium, flows from the posterior chamber of the eye through the pupil into the anterior chamber. Aqueous humor then leaves the anterior chamber and returns to the venous system by passing through the trabecular mesh of the anterior chamber into the Canal of Schlemm. A balance between production and absorption of aqueous humor maintains normal intraocular pressure (8-21 mm Hg). In chronic simple glaucoma, although the anterior chamber angle is open, an obstruction exists to the flow of the aqueous humor through the trabecular mesh. Acute glaucoma occurs if an obstruction, either complete or partial, in the flow of aqueous humor is produced by closure of the anterior chamber angle. This may result from an anteroposterior thickening of the lens or a forward movement of the lens that causes the iris to press against the lens capsule and thereby prevent outflow of aqueous humor.

MEDICAL MANAGEMENT

Beta Blockers: Timolol-use caution to patient with Asthma and CHF.

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Miotics: Pilocarpine-constrict the pupil and increase contraction of the ciliary muscle causing increased outflow of Aqueous humor. S/E: can cause blurred vision and browache.Sympathomimetics Mannitol

Epinephrine: reduces aqueous humor output; drug of choice to patient with asthma and CHF.Carbonic Anhydrase inhibitor: Acetazolamide: reduce aqueous production. S/E: nausea, malaise, numbness of extremities.

SURGICAL MANAGEMENT

Argon Laser Trabeculoplasty: A laser beam is focused through a gonio lens to make a series of burns in the trabecular meshwork allowing drainage.Cyclocryotherapy & cyclodiathermy: destroying parts of ciliary body to reduce aqueous humor production.Iredectomy: a surgery done on the eye, which in most cases is used to treat the condition called closed angle glaucoma.Sclerectomy: surgical removal of a part of the sclera.

NURSING MANAGEMENT

The medical and surgical management of glaucoma slows the progression of glaucoma but does not cure it. The lifelong therapeutic regimen mandates patient’s education. The nature of the disease and the importance of strict adherence to the medication

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regimen must be explained to ensure compliance. A thorough patient interview is essential to determine systemic conditions, current systemic and ocular medications, family history, and problems in compliance of medications.

PROPTOSIS

(EXOPHTHALMOS)

DEFINITION

Eye proptosis is a condition resulting in forward displacement and entrapment of the eye from behind by the

eyelids. The condition is also known as eye dislocation and eye luxation.

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Cavernous sinus thrombosis: This disorder usually causes sudden onset of pulsating unilateral exophthalmos. Accompanying it may be eyelid edema, decreased or absent pupillary reflexes, limited extraocular movement, and impaired visual acuity. Other features include high fever with chills, papilledema, headache, nausea, vomiting, somnolence and, rarely, seizures. Dacryoadenitis: Unilateral, slowly progressive exophthalmos is the most common sign of dacryoadenitis. Assessment may also reveal limited extraocular movement (especially on elevation and abduction), ptosis, eyelid edema and erythema, conjunctival injection, eye pain, and diplopia. Foreign body in the eye: When a foreign body enters the eye, exophthalmos may accompany other signs and symptoms of ocular trauma, such as eye pain, redness, and tearing. Hemangioma: Most common in young adults, this orbital tumor produces progressive exophthalmos, which may be mild or severe and unilateral or bilateral. Other signs and symptoms include ptosis, limited extraocular movement, and blurred vision. Hodgkin’s disease: In this disorder, unilateral exophthalmos may develop gradually along with eyelid edema, diplopia, and a palpable eyelid mass. More characteristic findings include painless swelling of one or more lymph nodes, intermittent fever, weight loss, fatigue, malaise, night sweats, hepatosplenomegaly, and pruritus. Lacrimal gland tumor: Exophthalmos usually develops slowly in one eye, causing its downward displacement toward the

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nose. The patient may also have ptosis and eye deviation and pain. Leiomyosarcoma: Most common in people ages 45 and older, this tumor is characterized by slowly developing unilateral exophthalmos. Other effects include diplopia, impaired vision, and intermittent eye pain. Leukemia: When leukemia causes intraorbital hemorrhage, mild to moderate bilateral exophthalmos and lacrimal gland enlargement also result. Associated signs and symptoms include bleeding tendency, fever, arthralgia, pallor, weakness, hepatosplenomegaly and, possibly, lymphadenopathy. Lymphangioma: Hemorrhage of this congenital tumor causes unilateral or bilateral exophthalmos, among other signs.Neuroblastoma: This highly malignant tumor, the most common extracranial solid tumor of childhood, may produce exophthalmos. Ocular tuberculosis: Occasionally, this rare disease causes progressive exophthalmos accompanied by ptosis, painless eyelid edema and erythema, and enlarged lacrimal glands. Examination may reveal yellow or white fat deposits on the cornea and small white nodules in the iris. Optic nerve meningioma: This tumor usually produces unilateral exophthalmos and a swollen temple. Impaired visual acuity, visual field deficits, and headache may occur.

SIGNS and SYMPTOMS

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Thus, a person presenting with abnormal protrusion of the eyes can have other associated symptoms such as fever, pain, redness as well as discharges in the event of an infection; eye pain, visual disturbances, headache in case of tumors and irritability, rapid pulse, excessive sweating and other thyroid symptoms in the event of a thyroid related problem. Apart from these, many other symptoms can be present in these patients and they will most often be subjected to ‘dry eyes’ as eye lids are unable to cover the surface of the eye which will expose the moist surface to outside dryness. In the event of serious underlying pathology, the blood supply to the eye or else the nerve which is responsible for the vision can get involved and thus has the potential to develop into complete blindness as well.

MEDICAL MANAGEMENT Treat the underlying cause, although treatment of Graves’ disease does not always improve ophthalmopathy, and radioactive iodine may make it worse; systemic steroids for acute flareups only Prevent eye injury and discomfort with artificial tears and sunglasses; may patch eye while sleeping Surgical decompression (in TAO and retrobulbar hemorrhage with acute optic neuropathy by direct compression or by increased intraocular pressure) If due to infectious causes, appropriate directed systemic intravenous antibiotic therapy and/or surgical debridement If due to noninfectious inflammation, administer systemic steroids or immunomodulating therapy, particularly if there

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is acute optic neuropathy Incisional or excisional biopsy of orbital tumors

NURSING MANAGEMENT 1. Prevent eye injury and discomfort with artificial tears and

sunglasses2. Protect the affected eye from trauma, especially drying of

the cornea.3. Don't place a gauze eye pad or other object over the affected

eye; removal could damage the corneal epithelium.4. If due to noninfectious inflammation, administer systemic

steroids or immunomodulating therapy, particularly if there is acute optic neuropathy

5. Because exophthalmos usually makes the patient self-conscious, provide privacy and emotional support.

6. If necessary, refer him to an ophthalmologist for a complete examination.

7. Prepare the patient for blood tests, such as a thyroid panel and a white blood cell count.

8. Teach ways to protect the eye from trauma, wind, and dust.9. Discuss the proper application of lubricants to the eye.10. Explain the underlying cause of the patient's exophthalmos

and its treatment.

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UVEITIS

DEFINITION

Uveitis specifically refers to inflammation of the middle layer of the eye, termed the "uvea" but in common usage may refer to any inflammatory process involving the interior of the eye.

CLINICAL DESCRIPTION

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Uveitis may be classified anatomically into anterior, intermediate, posterior and panuveitic forms, based on which part of the eye is primarily affected by the inflammation.

"Anterior uveitis" (or iridocyclitis) is the inflammation of the iris and anterior chamber. Anywhere from two-thirds to 90% of uveitis cases are anterior in location. This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature. Symptoms include red eye, injected conjunctiva, pain and decreased vision. Signs include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates ("KP") on the posterior surface of the cornea.

"Intermediate uveitis" (pars planitis) consists of vitritis - inflammatory cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana.

"Posterior uveitis" (or chorioretinitis) is the inflammation of the retina and choroid.

"Pan-uveitis" is the inflammation of all the layers of the uvea.

ETIOLOGY

Etiological classification including uveitis associated with trauma, infection, systemic disease, non-associated with a systemic disease and masquerade syndromes.

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Masquerade syndromes: are ophthalmic disorders that clinically present as either an anterior or posterior uveitis, but are not primarily inflammatory. The following are some of the most common:

Anterior segmentIntraocular foreign bodyJuvenile xanthogranulomaLeukemiaMalignant melanomaRetinal detachmentRetinoblastoma

Posterior segmentLymphomaMalignant melanomaMultiple sclerosisReticulum cell sarcomaRetinitis pigmentosaRetinoblastoma

SIGNS and SYMPTOMS

Redness of the eyeBlurred visionSensitivity to light (photophobia)

Dark, floating spots along the visual fieldEye pain

MEDICAL MANAGEMENT

Uveitis is typically treated with glucocorticoid steroids , either as topical eye drops (prednisolone acetate) or oral therapy with corticosteroids. But before giving corticosteroids, rule out corneal ulcers by Florescence Dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. In some

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cases an injection of PSTTA (posterior subtenontriamcinolone acetate) can also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatment with Infliximab or other anti-TNFs' infusions may prove helpful.

NURSING MANAGEMENT 1. Promote the patient's comfort by darkening the room

and telling him to close both eyes. Encourage use of sunglasses. Uveitis can cause photophobia.

2. Prepare the patient for diagnostic tests, such as corneal scraping and slit-lamp examination.

3. Administer eyedrops and ointments, as ordered. 4. Instruct patient to avoid coughing, bowing of head and

blowing of nose to prevent intra-occular pressure5. Teach the patient how to instill eyedrops or ointments. 6. Discuss ways to reduce the discomfort of photophobia. 7. Explain the disorder and treatment plan.

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DIABETIC RETINOPATHY

DEFINITION and ETIOLOGY

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of

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systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes.

Risk factors

All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset). The longer a person has diabetes, the higher the risk of developing some ocular problem. Between 40 to 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of retinopathy; however, these statistics were published in 2002 using data from four years earlier.

SIGNS and SYMPTOMS

Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause

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vision loss more rapidly, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.

As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (ocular hemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours.

These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs vision. In extreme cases, a person will only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.

On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of Clostridium novyi), and dot-blot hemorrhages.

Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens (hyperphacosorbitomyopicosis) as a result of sorbitol (sugar alcohol) accumulating in the lens. This edema often causes temporary myopia (nearsightedness). A common sign of hyperphacosorbitomyopicosis is blurring of distance vision while near vision remains adequate.

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DIAGNOSTIC TEST

Diabetic retinopathy is detected during an eye examination that includes:

Fluorescein angiography. In this test, a special dye is injected into the arm. Pictures are then taken as the dye passes through the blood vessels in the retina. This test allows the doctor to find the leaking blood vessels.Visual acuity test: This test uses an eye chart to measure how well a person sees at various distances (i.e., visual acuity).Pupil dilation: The eye care professional places drops into the eye to widen the pupil. This allows him or her to see more of the retina and look for signs of diabetic retinopathy. After the examination, close-up vision may remain blurred for several hours.Ophthalmoscopy: This is an examination of the retina in which the eye care professional: (1) looks through a device with a special magnifying lens that provides a narrow view of the retina, or (2) wearing a headset with a bright light, looks through a special magnifying glass and gains a wide view of the retina. Note that hand-held ophthalmoscopy is insufficient to rule out significant and treatable diabetic retinopathy.Optical coherence tomography (OCT): This is an optical imaging modality based upon interference, and analogous to ultrasound. It produces cross-sectional images of the retina (B-scans) which can be used to measure the thickness of the

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retina and to resolve its major layers, allowing the observation of swelling and or leakage.Digital Retinal Screening Programs: Systematic programs for the early detection of eye disease including diabetic retinopathy are becoming more common, such as in the UK, where all people with diabetes mellitus are offered retinal screening at least annually. This involves digital image capture and transmission of the images to a digital reading center for evaluation and treatment referral. See Vanderbilt Ophthalmic Imaging Center and the English National Screening Programme for Diabetic Retinopathy Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs for the early detection of diabetic retinopathy using slit-lamp biomicroscopy. These exist either as a standalone scheme or as part of the Digital program (above) where the digital photograph was considered to lack enough clarity for detection and/or diagnosis of any retinal abnormality.The eye care professional will look at the retina for early signs of the disease, such as: (1) leaking blood vessels, (2) retinal swelling, such as macular edema, (3) pale, fatty deposits on the retina (exudates) – signs of leaking blood vessels, (4) damaged nerve tissue (neuropathy), and (5) any changes in the blood vessels.

MEDICAL MANAGEMENT

There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease. In

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fact, even people with advanced retinopathy have a 90 percent chance of keeping their vision when they get treatment before the retina is severely damaged. These three treatments are laser surgery, injection of triamcinolone into the eye, and vitrectomy.

Although these treatments are very successful (in slowing or stopping further vision loss), they do not cure diabetic retinopathy. Caution should be exercised in treatment with laser surgery since it causes a loss of retinal tissue. It is often more prudent to inject triamcinolone. In some patients it results in a marked increase of vision, especially if there is an edema of the macula.

Intravitreal triamcinolone acetonide: Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity. The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect. Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis.Vitrectomy: Instead of laser surgery, some people require a vitrectomy to restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous. It involves removing the cloudy vitreous and replacing it with a saline solution.C-peptide: Though not yet commercially available, c-peptide has shown promising results in treatment of diabetic complications incidental to vascular degeneration. Once

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thought to be a useless byproduct of insulin production, it helps to ameliorate and reverse many symptoms of diabetes. Pine bark extract: A pine bark extract of oligomeric proanthocyanidins has been shown to improve microcirculation, retinal edema and visual acuity in the early stages of diabetic retinopathy.

NURSING MANAGEMENT Inform client about how the disease was formed.Teach client about proper diet; low sugar, low carbohydrates diet.Encourage to have proper exercise to loose weight.If patient is a smoker, advise to stop smoking.Provide safe environment for client since the vision has a problem, to prevent fall and injuries.If patient cannot see well, instruct significant others to organize their home and other things so that patient can easily find what he/she needs.Ensure that client is taking the medications correctly.Encourage compliance to medications and other treatments.instruct the S.O not to leave the unattended . to prevent fallsadminister antidiabetic medications as neededto treat underlying condition.

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HYPERTENSIVE RETINOPATHY

DEFNITION

Hypertensive retinopathy is damage to the retina due to high blood pressure.

CLINICA L

DESCRIPTION and ETIOLOGY

The retina is one of the "target organs" that are damaged by sustained hypertension. Subjected to excessively high blood pressure over prolonged time, the small blood vessels that involve the eye are damaged, thickening, bulging and leaking.

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Early signs of retinopathy correlate less well with mortality and morbidity than used to be thought, but signs of accelerated or "malignant" hypertension indicate severe illness.

SIGNS and SYMPTOMS

Most patients with hypertensive retinopathy present without visual symptoms, however, some may report decreased vision or headaches.

Signs of damage to the retina caused by hypertension include:

Arteriosclerotic changes: Arteriolar narrowing that is almost always bilateral. (The following grading system is specific to the degree of the arteriolar narrowing only. See later for the grading of hypertensive retinopathy as a whole.)

o Grade I - 3/4 normal calibero Grade II - 1/2 normal calibero Grade III - 1/3 normal calibero Grade IV - thread-like or invisible

Arterio-venous crossing changes (aka "AV nicking") with venous constriction and bankingArteriolar color changes Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width of the arteriole.

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Silver wire arterioles are those arterioles in which the central light reflex occupies all of the width of the arteriole.Vessel sclerosisIschemic changes (e.g. "cotton wool spots")Hemorrhages, often flame shaped.Edema Ring of exudates around the retina called a "macular star"Papilledema, or optic disc edema, in patients with malignant hypertensionVisual acuity loss, typically due to macular involvementDiabetic RetinopathyCollagen Vascular DiseaseAnemiaRadiation RetinopathyCentral Retinal Vein Occlusion

MEDICAL MANAGEMENT A major aim of treatment is to prevent, limit, or reverse such

target organ damage by lowering the pat essure. Anti-hypertensive treatment plays a major role in reversing ient's high blood pr the retinal changes. The eye is an organ where damage is easily visible at an early stage, so regular eye examinations are important.

NURSING MANAGEMENT 1. Inform client about how the disease was formed.2. Educate client how to control blood pressure.3. Plan the diet of the patient; low fat, low salt diet.4. If patient is a smoker, encourage to stop smoking.5. Monitor patient’s blood pressure regularly.6. If patient has a difficulty in seeing, assist the patient in

ambulation to prevent fall and injuries.

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7. Advice to increase nutritious food intake such as fruits and vegetables.

8. Advice to have a regular check up with the physician (when client is an out-patient)

9. Ensure that the patient is taking the drug prescribed regularly.

HYPEROPIA

DEFINITION

Hyperopia, or farsightedness, is a common vision problem, affecting about a fourth of the population. People with hyperopia can see distant objects very well, but have difficulty focusing on objects that are up close.

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CLINICAL DESCRIPTION

Hyperopia is a defect of vision caused by an imperfection in the eye (often when the eyeball is too short or the lens cannot become round enough), causing difficulty focusing on near objects, and in extreme cases causing a

sufferer to be unable to focus on objects at any distance. As an object moves toward the eye, the eye must increase its optical power to keep the image in focus on the retina. If the power of the cornea and lens is insufficient, as in hyperopia, the image will appear blurred. Hyperopia, and restoring of vision with convex lens.

People with hyperopia can experience blurred vision, asthenopia, accommodative dysfunction, binocular dysfunction, amblyopia, and strabismus.

Hyperopia is often confused with presbyopia, another condition that frequently causes blurry near vision. Presbyopes who report good far vision typically experience blurry near vision because of a reduced accommodative amplitude brought about by natural aging changes with the crystalline lens. It is also sometimes referred

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to as farsightedness, since in otherwise normally-sighted persons it makes it more difficult to focus on near objects than on far objects.

Classification of hyperopia

Hyperopia is typically classified according to clinical appearance, its severity, or how it relates to the eye's accommodative status.

Classification by clinical appearance

Simple hyperopiaPathological hyperopiaFunctional hyperopia

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ETIOLOGY

The causes of hyperopia are typically genetic and involve an eye that is too short or a cornea that is too flat, so that images focus at a point behind the retina. People with hyperopia can usually see distant objects well, but have trouble focusing on nearby objects.

This vision problem occurs when light rays entering the eye focus behind the retina, rather than directly on it. The eyeball of a farsighted person is shorter than normal.

Many children are born with hyperopia, and some of them "outgrow" it as the eyeball lengthens with normal growth.

SIGNS and SYMPTOMS

Farsighted people sometimes have headaches or eye strain and may squint or feel fatigued when performing work at close range. If you get these symptoms while wearing your eyeglasses or contact lenses, you may need an eye exam and a new prescription.

DIAGNOSTIC TEST

Visual acuity is affected according to the amount of hyperopia, as well as the patient's age, visual demands, and accommodative ability.

In severe cases of hyperopia from birth the brain has difficulty to merge the images that each individual eye see. This is

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because the images the brain receives from each eye is always blurred. A child with severe hyperopia has never seen objects in detail and might present with amblyopia or strabismus. If the brain never learns to see objects in detail, then there is a high chance that one eye will become dominant. The result is that the brain will block the impulses of the non-dominant eye with resulting amblyopia or strabismus. In contrast the child with myopia can see objects close to the eye in detail and does learn at an early age to see detail in objects.

The child with hyperopia will typically stand close, in front of a television. One would have expected that the child will stand far to see, but because the brain has never learned to see objects in detail and the child with hyperopia from birth presents with the picture of decreased visual perception.

The parents of a child with hyperopia do not always realize that the child has a problem at an early age. A hyperopic child might have problems with catching a ball because of blurred vision and because of a decreased ability to see three dimensional objects. The child will typically perform below average at school. As soon as a child starts identifying images a parent might find that the child cannot see small objects or pictures.

MEDICAL MANAGEMENT

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Various eye care professionals, including ophthalmologists, optometrists, orthoptists, and opticians, are involved in the treatment and management of hyperopia. At the conclusion of an eye examination, an eye doctor may provide the patient with an eyeglass prescription for corrective lenses.

Minor amounts of hyperopia are sometimes left uncorrected. However, larger amounts may be corrected with convex lenses in eyeglasses or contact lenses. Convex lenses have a positive dioptric value, which causes the light to focus closer than its normal range.

SURGICAL MANAGEMENT

Refractive surgery, such as LASIK or CK, is another option for correcting hyperopia. Surgery may reduce or eliminate your need to wear glasses or contact lenses. Investigational procedures involving corneal inlays and onlays may be a future option for correcting hyperopia.

NURSING MANAGEMENT

Introduce self to patient, and acknowledge visual impairment. This reduces patient’s anxiety.Orient patient to environment. Orientation reduces fear related to unfamiliar environment.Do not make unnecessary changes in environment. This ensures safety and maintains what the patient has arranged.

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Provide adequate lighting. The use of natural or halogen lighting is preferred to improve vision for patients with diminished vision.Place meal tray, tissues, water, and call light within patient’s range of vision or reach. These ensure safety and sense of independence.Communicate type and degree of impairment to all involved in patient’s care. This enhances continuity of care.Recommend use of visual aids when appropriate. Visual aids such as magnifying glass, large-type printed books, and magazines encourage reading.Place food on tray and plate in same place each meal and explain arrangement of food on tray and plate, using clockwise sequence. Encourage use of sense of touch. Touch encourages patient to become familiar with unfamiliar objects.Explain sounds or other unusual stimuli in environment. Explanations reduce fear.Encourage use of radios, tapes, and talking books. Diversional activities should be encouraged. Radio and television increase awareness of day and time.Remove environmental barriers to ensure safety. If furniture or wastebaskets are moved, notify patient of changes.Discourage doors from being left partially open. Fully open or closed doors reduce the risk for injury among the vision-impaired.Maintain bed in low position with side rails up, if appropriate. Side rails help remind patient not to get up

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without help when needed.Keep bed in locked position. This prevent falls.Guide patient when ambulating, if appropriate. Describe where you are walking; identify obstacles. Instruct patient to hold both arms of chair before sitting and to feel for the seat on chairs or sofas without arms. These reduce the risk of falls.Consult occupational therapy staff for assistive devices and training in their use. Supervise patient when smoking. Supervision prevents accidental fires.

DISEASES OF THE EARS

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OTITIS MEDIA

DEFINITION

Otitis media is inflammation of the middle ear, or a middle ear infection.It occurs in the area between the tympanic membrane and the inner ear, including a duct known as the eustachian tube. It is one of the two categories of ear inflammation that can underlie what is commonly called an earache, the other being otitis externa. Diseases other than ear

infections can also cause ear pain, including cancers of any structure that shares nerve supply with the ear and shingles which can lead to herpes zoster oticus. Though painful, otitis media is not threatening and usually heals on its own within 2–4 weeks.

CLINICAL DESCRIPTION

Otitis media has many degrees of severity, and various names are used to describe each. The terminology is sometimes

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confusing because of multiple terms being used to describe the same condition. A common misconception with ear infection is that sufferers think that a symptom is itchy ear. Although sufferers may feel discomfort, an itchy ear is not a symptom of ear infection.

CLASSIFICATION

1. Acute otitis media

Acute otitis media (AOM) is most often purely viral and self-limited, as is its usual accompanying viral URI (upper respiratory infection). There is congestion of the ears and perhaps mild discomfort and popping, but the symptoms resolve with the underlying URI. If the middle ear, which is normally sterile, becomes contaminated with bacteria, pus and pressure in the middle ear can result, and this is called acute bacterial otitis media. Viral acute otitis media can lead to bacterial otitis media in a very short time, especially in children, but it usually does not. The individual with bacterial acute otitis media has the classic "earache", pain that is more severe and continuous and is often accompanied by fever of 102 °F (39 °C) or more.[citation needed]. Bacterial cases may result in perforation of the ear drum, infection of the mastoid space (mastoiditis) and in very rare cases further spread to cause meningitis.

1st phase - exudative inflammation lasting 1–2 days, fever, rigors, meningism (occasionally in children), severe pain (worse at night), muffled noise in ear, deafness, sensitive mastoid process, ringing in ears (tinnitus)

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2nd phase - resistance and demarcation lasting 3–8 days. Pus and middle ear exudate discharge spontaneously and afterwards pain and fever begin to decrease. This phase can be shortened with topical therapy.

3rd phase - healing phase lasting 2–4 weeks. Aural discharge dries up and hearing becomes normal.

2. Serous Otitis media

Otitis media with effusion (OME), also called serous or secretory otitis media(SOM), is simply a collection of fluid that occurs within the middle ear space as a result of the negative pressure produced by altered Eustachian tube function. This can occur purely from a viral URI, with no pain or bacterial infection, or it can precede and/or follow acute bacterial otitis media. Fluid in the middle ear sometimes causes conductive hearing impairment, but only when it interferes with the normal vibration of the eardrum by sound waves. Over weeks and months, middle ear fluid can become very thick and glue-like (thus the name glue ear), which increases the likelihood of its causing conductive hearing impairment. Early-onset OME is associated with feeding while lying down and early entry into group child care, while parental smoking, too short a period of breastfeeding and greater amounts of time spent in group child care increased the duration of OME in the first two years of life.

3. Chronic suppurative otitis media

Chronic suppurative otitis media involves a perforation (hole) in the tympanic membrane and active bacterial infection within the

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middle ear space for several weeks or more. There may be enough pus that it drains to the outside of the ear (otorrhea), or the purulence may be minimal enough to only be seen on examination using a binocular microscope. This disease is much more common in persons with poor Eustachian tube function. Hearing impairment often accompanies this disease.

ETIOLOGY

Otitis media is most commonly caused by infection with viral, bacterial, or fungal pathogens. The most common bacterial pathogen is Streptococcus pneumoniae. Others include Pseudomonas aeruginosa, nontypeable Haemophilus influenzae, and Moraxella catarrhalis. Among older adolescents and young adults, the most common cause of ear infections is Haemophilus influenzae. Viruses such as respiratory syncytial virus (RSV) and those that cause the common cold may also result in otitis media by damaging the normal defenses of the epithelial cells in the upper respiratory tract.

A major risk factor for developing otitis media is Eustachian tube dysfunction, which leads to the ineffective clearing of bacteria from the middle ear.

The role of the anti-H. influenzae vaccine that children are regularly given is to prevent invasive disease such as meningitis and pneumonia. This vaccine is active only against strains of serotype b, which has been found to cause meningitis and pneumonia in children under five years, with children between 4 and 18 months the most susceptible. Isolates of serotype b rarely cause otitis media.

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Children younger than seven are much more prone to otitis media due to shorter eustachian tubes which are at a more horizontal angle than in the adult ear. They also have not developed the same resistance to viruses and bacteria as adults. Numerous studies have correlated the incidence in children with various factors such as nursing in infancy, bottle feeding when supine, parental smoking, diet, allergies, and automobile emissions; but the most obvious weakness of such studies is the inability to control the variable of exposure to viral agents during the studies[citation needed]. Breastfeeding for the first twelve months of life is associated with a reduction in the number, and duration of all OM infections. Pacifier use has been associated with more frequent episodes of AOM.

SIGNS AND SYMPTOMS

When the middle ear becomes acutely infected, pressure builds up behind the eardrum (tympanic membrane), frequently causing intense pain. It may result in bullous myringitis, in which the tympanic membrane is inflamed and blistered.

In severe or untreated cases, the tympanic membrane may rupture, allowing the pus in the middle ear space to drain into the ear canal. If there is enough of it, this drainage may be obvious. Even though the rupture of the tympanic membrane suggests a traumatic process, it is almost always associated with the dramatic relief of pressure and pain. In a simple case of acute otitis media in an otherwise healthy person, the body's defenses are likely to resolve the infection and the ear drum nearly always heals. Antibiotic

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administration can prevent perforation of the eardrum and hasten recovery of the ear.

Instead of the infection and eardrum perforation resolving, however, drainage from the middle ear can become a chronic condition. As long as there is active middle ear infection, the eardrum will not heal. The World Health Organization defines chronic suppurative otitis media (CSOM) as "a stage of ear disease in which there is chronic infection of the middle ear cleft, a non-intact tympanic membrane (i.e. perforated eardrum) and discharge (otorrhoea), for at least the preceding two weeks" (WHO 1998). (Notice WHO's use of the term serous to denote a bacterial process, whereas the same term is generally used by ear physicians in the United States to denote simple fluid collection within the middle ear behind an intact eardrum. Chronic otitis media is the term used by most ear physicians worldwide to describe a chronically infected middle ear with eardrum perforation.)

DIAGNOSTIC EXAMINATIONS

Acute otitis media is usually diagnosed via visualization of the tympanic membrane in combination with the appropriate clinical history. The use of a monocular otoscope and perhaps a tympanometer may not be able to distinguish bacterial versus viral etiology, especially if the canal is small and there is wax in the ear that obscures a clear view of the eardrum. Also, an upset child's crying can cause the eardrum to look inflamed due to distension of the small blood vessels on it, mimicking the redness associated with otitis media.

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The occurrence, duration, or severity of symptoms is not predictive of an ear infection in the absence of examination of the eardrum.

MEDICAL MANAGEMENT

Management of pain

To treat the pain caused by otitis media oral as well as topical analgesics are effective. Oral agents may include ibuprofen, acetaminophen, and / or narcotics. Topical agents shown to be effective include antipyrine and benzocaine ear drops.

Antibiotics

Many guidelines suggest deferring the start of antibiotics in acute bacterial otitis media for one to three days if pain is manageable with the above measures. This is recommended for a number of reasons including: two out of three children with acute otitis media resolve without antibiotic treatment, no adverse effect on long term outcomes have been found when treatment is withheld, antibiotics have significant rates of potential side effects, and a recent trial has found increased rates of recurrence of otitis in children who were treated with antibiotics.

The first line antibiotic treatment, if warranted, is amoxicillin. If the bacteria is resistant, then amoxicillin-clavulanate or another penicillin derivative plus beta lactamase inhibitor is second line. Five days of treatment has been found to be as effective as ten days in otherwise healthy children.

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Alternative therapies

There are claims that a variety of unproven techniques provide benefit to otitis media, including osteopathic and chiropractic manipulation, Eardoc, dietary exclusions, herbal supplements, acupuncture, traditional Chinese medicine, and homeopathy. The efficacy these alternative therapies can only be evaluated with randomised controlled trials with adequate sample sizes. None exist for otitis media: only anecdotal evidence is available.

SURGICAL MANAGEMENT

Myringotomy

If pain persists after antibiotic therapy and ear drums continue to bulge, a myringotomy (surgical opening of the pars tensa of the ear drum) is performed. A myringotomy drains middle-ear fluid and immediately relieves pain.

NURSING MANAGEMENT

Assess if the patient is taking some kind of drug. Other drug may cause otitis media as a side effect or toxicity effect if in long term use.

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Put the patient into a quiet environment to prevent occurrence of pain due to high pitched and loud sound, sound vibration in the ears, and stress. It also promotes relaxation.Put the patient in to bed rest to limit the head movement that intensify the pain.Apply heat or cold compress on affected site to relieve pain.Give soft foods to the patient as possible. Grinding of hard food may increase the muscle tension and pressure on the site.(PRE-OPERATIVE) Inform the patient that myringotomy is usually performed without anesthesia. (PRE-OPERATIVE) Discuss the procedure and purpose of myringotomy to the client to relieve anxiety and gain total cooperation and trust of the patient.(INTRA-OPERATIVE) Cleanse the ear cannal with povidone-iodine before the surgery to prevent incisional infection.(POST-OPERATIVE) Instruct the patient to maintain his head dry by not washing his/her hair for several days to prevent wound infection.(POST-OPERATIVE) Instruct the patient to avoid straining when he/she have a bowel movement. Over exertion increases muscle tension in the neck that can cause pain to the patient.

OTOSCLEROSIS

DEFINITION

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Otosclerosis formation of spongy bone around the structures of the middle and inner ear, leading to a low-tone hearing impairment.

CLINICAL DESCRIPTION

Approximately 0.5% of the population will eventually be diagnosed with otosclerosis. Post mortem studies show that as many as 10% of people may have otosclerotic lesions of their temporal bone, but apparently never had symptoms warranting a diagnosis. Caucasians are the most affected race, with the prevalence in the Black and Asian populations being much lower. In clinical practice otosclerosis is encountered about twice as frequently in females as in males, but this does not reflect the true sex ratio. When families are investigated it is found that the condition is only slightly more common in women. Usually noticeable hearing loss begins at middle-age, but can start much sooner. The hearing loss was believed to grow worse during pregnancy; but research shows that neither pregnancy nor breastfeeding may aggravate otosclerosis.

ETIOLOGY

Otosclerosis can result in conductive and/or sensorineural hearing loss. This usually will begin in one ear but will eventually affect both ears with a variable course.

SIGNS and SYMPTOMS

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On audiometry, the hearing loss is characteristically low-frequency, with higher frequencies being affected later. Sensorineural hearing loss (SNHL) has also been noted in patients with otosclerosis; this is usually a high-frequency loss, and usually manifests late in the disease.

DIAGNOSTIC TEST

Otosclerosis is traditionally diagnosed by characteristic clinical findings, which include progressive conductive hearing loss, a normal tympanic membrane, and no evidence of middle ear inflammation. The cochlear promontory may have a faint pink tinge reflecting the vascularity of the lesion, referred to as the Schwartze sign. Conductive hearing loss is usually secondary to impingement of abnormal bone on the stapes footplate. This involvement of the oval window forms the basis of the name fenestral otosclerosis. The most common location of involvement of otosclerosis is the bone just anterior to the oval window at a small cleft known as the fissula ante fenestram. The fissula is a thin fold of connective tissue extending through the endochondral layer, approximately between the oval window and the cochleariform process, where the tensor tympani tendon turns laterally toward the malleus.

Imaging is usually not pursued in those with uncomplicated conductive hearing loss and characteristic clinical findings. Those with only conductive hearing loss are often treated medically or with surgery without imaging. The diagnosis may be unclear clinically in cases of sensorineural or mixed hearing loss and may become apparent only on imaging. Therefore, imaging is often performed

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when the hearing loss is sensorineural or mixed. The mechanism of sensorineural hearing loss in otosclerosis is less well understood. It may result from direct injury to the cochlea and spiral ligament from the lytic process or from release of proteolytic enzymes into the cochlea.

High-resolution CT shows very subtle bone findings. It is the imaging technique of choice particularly with the advent of better and higher-resolution CT techniques.

Otosclerosis on CT can be graded using the grading system suggested by Symons and Fanning. Grade 1, solely fenestral; grade 2, patchy localized cochlear disease (with or without fenestral involvement) to either the basal cochlear turn (grade 2A), or the middle/apical turns (grade 2B), or both the basal turn and the middle/apical turns (grade 2C); and grade 3, diffuse confluent cochlear involvement (with or without fenestral involvement).

PATHOPHYSIOLOGY

The pathophysiology of otosclerosis is complex. The key lesions of otosclerosis are multifocal areas of sclerosis within the endochondral temporal bone. These lesions share some characteristics with Paget’s Disease, but they are not thought to be otherwise related. Histopathologic studies have all been done on cadaveric temporal bones, so only inferences can be made about progression of the disease histologically. It seems that the lesions go through an active “spongiotic” / hypervascular phase before developing into “sclerotic” phase lesions. There have been many

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genes and proteins identified that, when mutated, may lead to these lesions. Also there is mounting evidence that measles virus is present within the otosclerotic foci, implicating an infectious etiology (this has also been noted in Paget’s Disease).

CHL in otosclerosis is caused by two main sites of involvement of the sclerotic (or scar-like) lesions. The best understood mechanism is fixation of the stapes footplate to the oval window of the cochlea. This greatly impairs movement of the stapes and therefore transmission of sound into the inner ear (“ossicular coupling”). Additionally the cochlea’s round window can also become sclerotic, and in a similar way impair movement of sound pressure waves through the inner ear (“acoustic coupling”).

SNHL in otosclerosis is controversial. Over the past century, leading otologists and neurotologic researchers have argued whether the finding of SNHL late in the course of otosclerosis is due to otosclerosis or simply to typical presbycusis. There are certainly a few well documented instances of sclerotic lesions directly obliterating sensory structures within the cochlea and spiral ligament, which have been photographed and reported post-mortem. Other supporting data includes a consistent loss of cochlear hair cells in patients with otosclerosis; these cells being the chief sensory organs of sound reception. A suggested mechanism for this is the release of hydrolytic enzymes into the inner ear structures by the spongiotic lesions.

MEDICAL MANAGEMENT

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One of the medical management includes Fluoride administration, which theoretically becomes incorporated into bone and inhibits otosclerotic progression. This treatment cannot reverse conductive hearing loss, but may slow the progression of both the conductive and sensorineural components of the disease process. Otoflour is one such widely used medicine, comprising sodium fluoride. Recently, some success has been reported with bisphosphonate medications, that inhibit bone destruction.

SURGICAL MANAGEMENT

Treatment of otosclerosis relieves on two primary options: hearing aids (more recently including bone-conduction hearing aids) and a surgery called a stapedectomy.

Hearing aids are usually very effective early in the course of the disease, but eventually a stapedectomy may be required for definitive treatment. Early attempts at hearing restoration via the simple freeing the stapes from its sclerotic attachments to the oval window were met with temporary improvement in hearing, but the conductive hearing loss would almost always recur. A stapedectomy consists of removing a portion of the sclerotic stapes footplate and replacing it with an implant that is secured to the incus. This procedure restores continuity of ossicular movement and allows transmission of sound waves from the eardrum to the inner ear. A modern variant of this surgery called a stapedotomy, is performed by drilling a small hole in the stapes footplate with a micro-drill or a laser, and the insertion of a piston-like prothesis. The success rate of

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either a stapedotomy or a stapedectomy depends greatly on the skill and the familiarity with the procedure of the surgeon.

NURSING MANAGEMENT (POST-OPERATIVE)

Instruct patient to avoid straining when he/she have bowel movement.

Instruct patient not to drink via straw for 2-3 weeks.Instruct patient to avoid air travel for 2 to 3 weeks.Instruct patient to avoid excessive coughing for 2-3 weeks.Instruct patient to avoid people with colds to prevent infection.Inform patient not to wet or wash the hair or taking shower for a week.Inform patient to avoid rapid moving of head, bouncing, and bending over for 3 weeks.Teach the patient in keeping the ear dry by placing cotton balls coated with petroleum jelly in the ear. Change the cotton ball daily. Petroleum jelly prevents moisture from developing inside the ear canal.If blowing the nose, teach patient to blow gently, one side at a time, with his/her mouth open to prevent development of muscle pressure in the buccal cavity and the ear site.Report excessive drainage immediately to the physician for proper management.

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OTITIS EXTERNA

DEFINITION

Otitis externa refers to an infection of the ear canal (outer ear), the tube leading from the outside opening of the ear in towards the ear drum. The infection usually

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develops in children and adolescents whose ears are exposed to persistent, excessive moisture.

CLINICAL DESCRIPTION

The external ear canal is a tube approximately 1 in (2.5 cm) in length that runs from the outside opening of the ear to the start of the middle ear, which is behind the tympanic membrane (ear drum). The canal is partly cartilage and partly bone. The lining of the ear canal is skin, which is attached directly to the covering of the bone. Glands within the skin of the canal produce a waxy substance called cerumen (popularly called earwax). Cerumen is designed to protect the ear canal, repel water, and keep the ear canal too acidic to allow bacteria to grow.

Continually exposing the ear canal to moisture may cause significant loss of cerumen. The delicate skin of the ear canal, unprotected by cerumen, retains moisture and becomes irritated. Without cerumen, the ear canal stops being appropriately acidic, which allows for the growth of microorganisms. Thus, the warm, moist, dark environment of the ear canal becomes a hospitable environment for development of an infection.

Otitis externa is commonly referred to as swimmer's ear.

ETIOLOGY

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Traumatized external canal (particularly due to cotton-tipped swabs)Bacterial infectionPseudomonas species (38% of all cases)1 Staphylococcus speciesGram-negative rodsFungal infection (rare, 10%) -Aspergillus speciesYeast (rare) -Candida speciesEczematous otitis externaEczema

SeborrheaNeurodermatitisContact dermatitis from earrings or hearing aid usePurulent otitis media with perforation of the tympanic membrane and drainage (This may mimic findings in otitis externa, but it is usually painless and has no swelling of the canal.)Sensitivity to topical medications

SIGNS and SYMPTOMS

In general, a history of 1-2 days of progressive ear painFrequently, a history of exposure to or activities in water, such as swimming, surfing, and kayakingPruritus within the ear canalPurulent dischargeConductive hearing lossFeeling of fullness or pressurePhysical

The sine qua non of otitis externa is pain on gentle traction of the external ear structures.Periauricular adenitis may occur but is not necessary for the diagnosis.Examination of the canal reveals erythema, edema, and narrowing of the external auditory canal.

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Typically, accumulation of moist debris is observed in the external canal.The tympanic membrane may be difficult to visualize and may be mildly inflamed, but it should be normally mobile on insufflation.Spores and hyphae may be seen in the external canal if the etiology is fungal.

Eczema of the pinna may be present.By definition, cranial nerve (CN) involvement (ie, of CNs VII and IX-XII) is not associated with simple otitis externa.

DIAGNOSTIC TEST Visualization of the outer ear is the mosat accurate

diagnostic examnation for Otitis externa.

PATHOPHYSIOLOGY

The ear canal guards against infection by producing a protective layer of cerumen, which creates an acidic and lysozyme-rich environment. While a paucity of cerumen allows for bacterial growth, an excess can cause retention of water and debris, which can create an environment ideal for bacterial invasion. This may happen when the ear canal is regularly exposed to water as seen in swimmers and divers. Localized trauma from foreign objects placed in the ear can also lead to direct bacterial invasion in the ear canal.

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Once an infection becomes established, localized maceration and inflammation occur, which lead to symptoms.

Rarely, the bacterial infection can invade the deeper underlying structures of the soft tissue and destroy the underlying temporal bone. This is called malignant otitis externa and is a complication seen more often in immunocompromised patients.

MEDICAL and OTHER MANAGEMENT

Antibiotics: Neomycin, polymixin .Steroids: hydrocortisone.A wick maybe inserted. (Absorptive material placed into and extending out of the canal).Acid solution: distilled vinegar & isopropyl alcohol. Mullein (Verbascum thapsus) oil has anti-inflammatory properties and may be apppied to the infected ear canal (one to three drops every three hours) to help soothe and heal the ear. Garlic (Allium sativum) is a natural antibiotic. Garlic juice can be combined with equal parts of glycerin and a carrier oil such as olive or sweet olive and applied (one to three drops) to the infected ear every three hours.

NURSING MANAGEMENT

Instruct in swimming in polluted water and in pools or hot tubs without good chlorine and pH control should be

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avoided.Before swimming, a protective coating consisting of several drops of mineral oil, baby oil, or lanolin can be applied to the ear canal.Keeping the ear dry. After swimming, several drops of a mixture of isopropyl alcohol and white vinegar can be put into the ear canal to ensure that it dries adequately.Instruct that outer ear should be cleaned wiped with a clean washcloth. The use of pointed objects to dig into the ear canal, especially those that can scratch the skin, should be avoided.

LABYRINTHITIS

DEFINITION

Labyrinthitis is an inflammation of the inner ear. It derives its name from the labyrinths that house the vestibular system (which

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sense changes in head position). Labyrinthitis can cause balance disorders.

CLINICAL DESCRIPTION

In addition to balance control problems, a labyrinthitis patient may encounter hearing loss and tinnitus. Labyrinthitis is usually caused by a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy or as a reaction to a particular medication. Both bacterial and viral labyrinthitis can cause permanent hearing loss, although this is rare.

Labyrinthitis often follows an upper respiratory tract infection (URI).

TYPES OF LABYRINTHITIS

Serous (viral) labyrinthitis:

Caused by inflammation of the labyrinth only.bTypically presents with less severe hearing loss and vertigo than suppurative labyrinthitis; hearing loss often recovers.hearing loss, whereas patients with viral labyrinthitis have hearing loss.

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Suppurative (bacterial) labyrinthitis:

Follows direct bacterial invasion of the inner earTypically presents with severe to profound hearing loss and vertigo.Meningogenic labyrinthitis:Occurs in the setting of meningitisTypically begins at the basal turn of the cochlea adjacent to the opening of the cochlear aqueduct.

Autoimmune labyrinthitis:

Autoimmune conditions (e.g., Cogan's syndrome or Behcet's disease) affecting the labyrinth typically present with bilateral simultaneous or sequential hearing loss and vertigoCan be corticosteroid responsive, but sometimes progress to bilateral profound hearing loss and vestibular hypo-function.

Labyrinthitis ossificans:

Fibrosis of the membranous labyrinth occurs within a few days of acute infectionOssification can occur as early as fibrosis, resulting in complete osseous replacement of the membranous labyrinthMembranous labyrinth can be obstructed in up to 30% of patients with suppurative labyrinthitis.

Syphilitic labyrinthitis:

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Can follow tertiary neurosyphilis, which occurs many years after primary syphilis infection, and is not seen with acute primary or secondary syphilis Patients can present with progressive hearing loss and pressure- or sound-induced vertigo (Hennebert and Tullio signs).HIV-associated labyrinthitis:A variety of auditory and vestibular complaints, including labyrinthitis, have been reported in patients with AIDS. The relative importance of the HIV infection itself as opposed to its associated opportunistic infections requires further study.

ETIOLOGY

Many times, you cannot determine the cause of labyrinthitis. Often, the condition follows a viral illness such as the color and 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:

Fluid to collect in the labyrinth (serous labyrinthitis) Fluid to directly invade the labyrinth, causing pus-producing (suppurative) labyrinthitisAllergies Alcohol abuse

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A benign tumor of the middle ear Certain medications taken in high doses Furosemide (Lasix)

AspirinSome IV antibiotics Phenytoin (Dilantin) at toxic levels

SIGNS and SYMPTOMS

Vertigo Nausea Vomiting Loss of balance

A mild headache Tinnitus (a ringing or rushing noise) 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. 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. Rarely, the condition may last all your life, as with Meniere's disease. This condition usually involves tinnitus and hearing loss with the vertigo. In rare cases it can be debilitating.

DIAGNOSTIC TEST

A complete physical and neurological exam should be done. An ear examination may not reveal any problems.

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Usually, the diagnosis of layrinthitis does not require other tests. Tests will be done to rule out other causes for your symptoms. These may include:

EEGElectronystagmographyHead CT scanHearing tests (audiology/audiometry)

MRI of the headWarming and cooling the inner ear with air or water (caloric stimulation) to test eye reflexes

MEDICAL MANAGEMENT

Labyrinthitis usually goes away within a few weeks. Treatment involves reducing symptoms, such as spinning sensations. Medications that may reduce symptoms include:

AntihistaminesCorticosteroids such as prednisone when symptoms are severeMedicines such as compazine to control nausea and vomitingMedicines to relieve dizziness such as meclizine or scopalamineSedative-hypnotics such as ValiumPersistent balance problems may improve with physical therapy. To prevent worsening of symptoms during episodes of labyrinthitis, try the following:Keep still and rest when symptoms occur.Gradually resume activity.Avoid sudden position changes.Do not try to read when symptoms occur.Avoid bright lights.

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Therapeutic maneuvers such as the Epley maneuver, if the doctor thinks benign positional vertigo-tiny stones bouncing around in the labyrinth-may be the cause. The Epley maneuver, developed by Dr. John Epley, is a movement of your head to move the stones a certain way to end the dizziness.

NURSING MANAGEMENT

When cleaning ear of debris, or to soak up any drainage, a wick may be fashioned of cotton balls or absorbent towels. Care should be taken if using Q-tips (cotton swabs) in order to prevent abrasions to the tissue in the ear, and the packing of wax or debris against the ear drum. Give medications for the length of time prescribed. When administering topical agents: instill medicine, gently hold ear closed, and massage ear canal 30 to 60 seconds to ensure dispersion of medication. Maintain clean cage environment. Maintain safe environment particularly if head tilt is severe. Keep food and water within easy access to rat. Provide high calorie foods (e.g., avocado), or food supplements such as Nutri-Cal Paste, canned Ensure, soy or soy formula, along with a multi-vitamin and mineral supplement (can be found in pet store) if weight loss or food intake is poor. Contact veterinarian if infection worsens or does not resolve, or if there is decreased appetite and weight loss.

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MÉNIÈRE'S DISEASE

DEFINITION

Ménière's disease is a disorder of the inner ear that can affect hearing and balance to a varying

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degree. It is characterized by episodes of vertigo and tinnitus and progressive hearing loss, usually in one ear. It is named after the French physician Prosper Ménière, who, in an article published in 1861, first reported that vertigo was caused by inner ear disorders. The condition affects people differently; it can range in intensity from being a mild annoyance to a chronic, lifelong disability.The symptoms of Ménière's are variable; not all sufferers experience the same symptoms.

CLINICAL DESCRIPTION

Meniere's disease most often affects adults between the ages of 40 to 60. Isolated symptoms can appear between ages 20and 60. It is uncommon for people older than age 60 to develop Meniere's disease. Approximately 40,000 new cases of Meniere's disease are diagnosed annually in the United States. Only about 3% of patients diagnosed with Meniere's disease are children. Male to female ratio ranges from equal to a slight preponderance of females over males. Some women report improvement of symptoms following pregnancy. In approximately 5% of cases of Meniere's disease, there is a positive family history for the condition indicating that there is a genetic component in a subset of individuals with Meniere's disease. Although most cases of Meniere's disease are unilateral, approximately 10-50% of patients also develop symptoms in the opposite ear. There is no predominance of right or left ear.

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ETIOLOGY

Viruses

Herpes virus (HSV) antibodies are found more commonly in Meniere's patients (Arnold and Niedermeyer, 1997). On the other hand, others have not found viral DNA from herpes simplex, CMV or varicella zoster in the vestibular ganglion (Welling et al, 1997). Otosyphilis can produce a clinical picture identical to Meniere's. Pulec indicated that syphilis is the cause of Meniere's disease in 6% of all cases (1997). This is much higher than the author's experience in whom certainly less than 1% of all patients have a positive FTA for syphilis.

Hereditary predisposition

About one in three patients with Menieres disease have a first-degree relative with Menieres disease. In theory, hereditary predisposition might be related to differences in anatomy of fluid channels within the ear or differences in immune response.

Autoimmune disorders

About 60% of patients with Meniere's disease have serum antibodies for inner ear proteins. About 10% of Meniere's patients have well documented autoimmune disorders (but the general population also has a high prevalence of these disorders). Some Meniere's patients show evidence for a

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change in their immunity around the time of their attacks (Mamikoglu et al, 2002).

Head injury

There are clearly cases of post-traumatic Meniere's syndrome. These cases are attributed to hydrodynamic changes caused by scarring from bleeding into the inner ear.

SIGNS and SYMPTOMS

According to the American Academy of Otolaryngology-Head and Neck Surgery, Meniere's disease is characterized by four major symptoms which occur with varying degrees of intensity:

Vertigo - an intense sense of spinning. This is usually episodic and can range from mild to severe. The vertigo attacks of Meniere's disease are rotational and the duration of each episode must be at least 20 minutes in order to be classified as Meniere's disease.Hearing loss - fluctuating low-frequency sensorineural hearing loss that becomes worse during attacks and may permanently deteriorate over time.Tinnitus - typically a low tone ringing or roaring noise in the ears.Aural fullness - a sense of fullness in the ear.

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DIAGNOSTIC TEST

Doctors establish a diagnosis with complaints and medical history. However, a detailed otolaryngological examination, audiometry and head MRI scan should be performed to exclude a tumour of the eighth cranial nerve or superior canal dehiscence which would cause similar symptoms. Because there is no definitive test for Ménière's, it is only diagnosed when all other causes have been ruled out. Because Ménière's, by definition, is idiopathic, one no longer has Ménière's disease if the cause of the symptoms has been discovered.

MEDICAL MANAGEMENT Antihistamines considered antiemetics such as meclozine and dimenhydrinateAntiemetic drugs such as trimethobenzamide.Antivertigo/antianxiety drugs such as betahistine and diazepam.Herbal remedies such as ginger root.

SURGICAL MANAGEMENT

Is that are available for patients with Meniere's disease who experience severe, unremitting episodes of vertigo that cannot be controlled with more conservative treatments. These surgical treatments include:

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Endolymphatic sac surgery

LabyrinthectomyVestibular neurectomy

NURSING MANAGEMENT

Reduce or minimize environmental noise. Reduce noise so that speaker does not have to compete to be heard.Face patient in good light and keep hands away from mouth. This enhances patient’s use of lip-reading, facial expressions, and gesturing.Speak close to patient’s "better" ear, as appropriate.Avoid shouting or yelling. This prevents humiliation.Use simple language and short sentences.Speak slowly.

HEARING LOSS

CLINICAL DESCRIPTION

Hearing loss, or hearing impairment (say: im-pare-ment), happens when there is a problem with one or more parts of the ear or ears. Someone who has hearing loss or impairment may be able to hear some sounds or nothing at all. Impairment means something is not

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working correctly or as well as it should. People also may use the words deaf, deafness, or hard of hearing when they're talking about hearing loss. A hearing loss exists when an animal has diminished sensitivity to the sounds normally heard by its species. In humans, the term hearing impairment is usually reserved for people who have relative insensitivity to sound in the speech frequencies. The severity of a hearing loss is categorized according to the increase in volume that must be made above the usual level before the listener can detect it. In profound deafness, even the loudest sounds that can be produced by an audiometer (an instrument used to measure hearing) may not be detected.

Another aspect to hearing involves the perceived clarity of a sound rather than its amplitude. In humans, that aspect is usually measured by tests of speech perception. These tests measure one's ability to understand speech, not to merely detect sound. There are very rare types of hearing impairments which affect speech understanding alone

TYPES OF HEARING LOSS

Conductive hearing loss

It is due to any condition that interferes with the transmission of sound through the outer and middle ear to the inner ear. This type of hearing loss can be successfully treated in most cases.

Sensorineural hearing loss

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Is the damage lies in the inner ear, the acoustic nerve, or both. Most physicians call this condition "nerve deafness."

"Neural" hearing loss is the correct term to use when the damage is in the acoustic nerve, anywhere between its fibers at the base of the hair cells and the relay stations in the brain (the auditory nuclei). Other common names for this type of loss are "nerve deafness" and "retrocochlear" hearing loss.

Central hearing loss

The problem lies in the central nervous system, at some point within the brain. Interpreting speech is a complex task. Some people can hear perfectly well but have trouble interpreting or understanding what is being said. Although information about central hearing loss is accumulating, it remains somewhat a mystery in otology (the medical specialty of ear medicine and surgery).

A condition called central auditory processing disorder frequently leads people to think they have hearing loss when their hearing is actually normal. Despite the fact that this problem is extremely common and present in many highly successful people, it is actually classified as a learning disability.

Functional Hearing Loss

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It involves a psychological or emotional problem, rather than physical damage to the hearing pathway. Individuals with this type of hearing loss do not seem to hear or respond; yet, in reality, they have normal hearing.

The most important challenge for physicians is to classify this condition properly. It may be difficult to determine the specific emotional cause, but if the classification is made accurately, the proper therapy can begin.

Too often, a functional hearing loss is not recognized, and individuals receive useless treatments for prolonged periods. In turn, this process may aggravate the emotional element and cause the condition to become more resistant to treatment.

Mixed Hearing Loss

Frequently, a person experiences two or more types of hearing impairment, and this is called mixed hearing loss. This term is used only when both conductive and sensorineural hearing losses are present in the same ear. However, the emphasis is on the conductive hearing loss, because available therapy is so much more effective for this disorder.

ETIOLOGY

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There are 2 basic types of hearing loss, which are called conductive and sensorineural.

CONDUCTIVE CAUSES: Conductive hearing losses result from physical problems with the movement of the sound wave through the ear. A simple example is blockage of the ear canal.

Obstructed external ear canal - Cerumen (wax) build-up, hematoma (blood collection), or foreign body in the ear canal. This is one of the most common causes of hearing loss and the easiest to fix. Perforated tympanic membrane - Caused by direct trauma such as a finger or cotton swab, middle-ear infections (otitis media), or explosions (blast injury) Dislocated ossicle (malleus, incus, or stapes) - Usually from trauma to the ear Otitis media - Middle ear infection .Otitis externa - Infection of the ear canal that causes it to swell.

Sensorineural causes: Sensorineural causes are from damage to the hair cells or nerves that sense sound waves.

Acoustic trauma - Prolonged exposure to loud noises causes the hair cells on the cochlea to become less sensitive. Barotrauma (pressure trauma) or ear squeeze - Usually in divers Head trauma - A fracture of the temporal bone can disrupt the nerves of the auditory system

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Ototoxic drugs - Certain drugs can affect hearing by damaging the nerves involved in hearing. Usually this occurs when large or toxic doses are used but may also occur with lower doses. Acoustic neuroma - A tumor in the auditory nerve. Usually associated with ringing in the ears. Aging (presbycusis)

Infections

o Mumps o Measles o Influenza o Herpes simplex o Herpes zoster

o Mononucleosis o Syphilis o Meningitis

SIGNS and SYMPTOMS

Hearing loss may be gradual or sudden. Hearing loss may be very mild, resulting in minor difficulties with conversation, or as severe as complete deafness. The speed with which hearing loss occurs may give clues as to the cause.

If hearing loss is sudden, it may be from trauma or a problem with blood circulation. A gradual onset is suggestive of other causes such as aging or a tumor.

If you also have other associated neurological problems, such as tinnitus (ringing in the ears) or vertigo (spinning sensation), it may indicate a problem with the nerves in the ear or brain.

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Hearing loss may be unilateral (only 1 ear) or bilateral (both ears). Unilateral hearing loss is most often associated with conductive causes, trauma, and acoustic neuromas.

Pain in the ear is associated with ear infections, trauma, and obstruction in the canal. Ear infections may also cause a fever.

DIAGNOSTIC EXAMINATIONS

In most medical offices or in the emergency department, doctors do not have access to equipment to directly test your hearing (an audiometer). In these settings the doctor will most likely evaluate your hearing with a tuning fork. The examination may include the following:

Each ear will be tested separately to see if you can hear the sound coming from a tuning fork.The ear canal and tympanic membrane will be inspected with an otoscope (a special instrument with a light and a tip to look into the ear canal).The nose, nasopharynx (the part of your throat that your ears drain into, located just above your soft palate), and upper respiratory tract usually will be carefully examined.A general neurologic exam, which includes tests of the nerves that control movement, sensation, and reflexes, will be done.If a process inside the brain (such as an acoustic neuroma) is suspected, a CT scan of the brain may be performed.

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If an infection, vascular problem, or drug interaction is suspected, blood tests may be performed.Tympanometry may be indicated if a problem with the tympanic membrane (eardrum) is suspected. This test evaluates the middle ear’s ability to receive sound waves.

MEDICAL TREATMENT

If a foreign body is found in the ear canal, the doctor will try to take it out. It can be removed by flushing the canal with water, using suction, or using forceps.Cerumen (earwax) in the canal is removed by flushing the canal or scooping out the wax with special instruments. If the wax is too hard to remove, the doctor may prescribe softening drops (also available over-the-counter) and have you return in a week to try to remove it again.If infection is found, antibiotics will most likely be prescribed. Middle ear infections usually require pills, while infections of the ear canal can usually be treated with eardrops. If the eardrum is perforated from an injury, no medicines will usually be prescribed. A follow-up visit with the same doctor or an ear, nose, and throat specialist (otolaryngologist or ENT) will be suggested. Eardrum perforation from an infection is usually treated with antibiotics. If a problem is suspected with the bones of the middle ear or nerves, a referral will likely be made to a specialist such as an ear, nose, and throat specialist. If the cause of the hearing loss is due to medications, the medication will be stopped or changed.

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If there is a tumor, such as an acoustic neuroma, a referral to a neurosurgeon (a surgeon specializing in brain, spinal cord, or nerve surgery) or ear, nose, and throat specialist will be made. If associated symptoms are troublesome (tinnitus, vertigo), anti-anxiety or motion sickness medication may be prescribed. If Ménière disease is the suspected cause, antihistamines or nicotinic acid can sometimes be helpful. A low-salt diet may also be suggested.

NURSING INTERVENTIONS

Use touch and eye contact. These gain patient’s attention.

When speaking, do the following: Reduce or minimize environmental noise. Reduce noise so that speaker does not have to compete to be heard.Face patient in good light and keep hands away from mouth. This enhances patient’s use of lip-reading, facial expressions, and gesturing.Speak close to patient’s "better" ear, as appropriate.Avoid shouting or yelling. This prevents humiliation.Use simple language and short sentences.Speak slowly.

Use grease boards, computers, or other writing tools. These help communicate with profoundly hearing-impaired individuals.

For patients with hearing aid(s), ensure that hearing aid(s) is in place, clean and working. Patients with new hearing aid(s) need time to adjust to the sound produced.

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Encouragement is often needed, especially among elderly patients who may decide that the hearing aid(s) is not worth the effort.

Provide encouragement to use hearing aid(s).

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