Msn Sensory Disturbances

ASSESSING CLIENTS WITH EYE DISORDERS REVIEW OF ANATOMY AND PHYSIOLOGY The Eye and Vision The eyes are complex structures, containing 70% of the sensory receptors of the body. Each eye is a sphere measuring about 1 in (2.5cm) in diameter, surrounding and protected by a bony orbit and cushions of fat. The primary functions of the eye are to encode the patterns of light from the environment through photoreceptors and to carry the coded information from the eyes to the brain. The brain gives meaning to the coded information, allowing us to make sense of what we see. Both extraocular and intraocular structures are considered a part of the eye. Extraocular Structures Extraocular or accessory structures of the eye are those portions of the eye outside the eyeball yet vital to its protection. These structures are the eyebrows, the eyelids, the eyelashes, the conjuctiva, the lacrimal apparatus, and the extrinsic eye muscles. The eyebrows are short, coarse hairs located above the eyes over the superior orbital ridges of the skull. The eye brows shade the eyes and keep perspiration away from them. The eyelids are thin, loose folds of skin covering the anterior eye. They protect the eye from foreign bodies, regulate the entry of light into the eye, and distribute tears by blinking. The eyelashes are short hairs that project from the top and bottom borders of the eyelids. When anything touches the eyelashes, the blinking reflex is initiated to protect the eyes from foreign objects. The conjunctiva is a thin, transparent membrane that lines the inner surfaces of the eyelids and also folds over the anterior surface of the eyeball. The palpebral conjuctiva lines the upper and lower eyelids, whereas the bulbar conjuctiva loosely covers the anterior sclera (the white part of the eye ). The conjuctiva is a mucous membrane that lubricates the eyes. The lacrimal apparatus is composed of the lacrimal gland, the puncta, the lacrimal sac, and the nasolacrimal duct. Together, these structures secrete, distribute, and drain tears to cleanse and moisten the eye’s surface. The six extrinsic eye muscles control the movement of the eye, allowing it to follow a moving object. The muscles also help maintain the shape of the eyeball.

INTRAOCULAR STRUCTURES The intraocular structures transmit visual images and maintain homeostasis of the inner eye. Those lying in the anterior portion of each eyeball are the sclera and the cornea (forming the outermost coat of the eye, call the fibrous tunic), the iris, the pupil, and the anterior cavity. The white sclera lines the outside of the eyeball. The functions of the sclera are to protect and give shape to the eyeball. The sclera gives way to the cornea over the iris and pupil. The cornea is transparent, avascular and very sensitive to touch. The cornea forms a window that allows light to enter the eye and is a part of its light-bending apparatus. When the cornea is touched, the eyelids blink and tears are secreted. The iris is a disc of muscles tissue surrounding the pupil and lying between the cornea and the lens. The iris gives the eye its color and regulates light entry by controlling the size of the pupil. The pupil is the dark center of the eye through which light enters. The pupil constricts when bring light enters the eye and when it is used for near vision; it dilates when light conditions are dim and when eye is used for far vision. In response to intense light, the pupil constricts rapidly in the papillary light reflex. The anterior cavity is made up of the anterior chamber (the space between the cornea and the iris) and the posterior chamber (the space between the iris and the lens). The anterior cavity is filled with a clear fluid called the aqueous humor. Aqueous humor is constantly formed and drained to maintain a relatively constant pressure of from 15-20 mm Hg in the eye. The Canal of Schlemm, a network of channels that circle the eye in the angle at the junction of the sclera and the cornea, is the drainage system for fluid moving between the anterior and posterior chambers. Aqueous humor provides nutrients and oxygen to the cornea and lens. The intraocular structures that lie in the internal chamber of the eye are the posterior cavity and vitreous humor, the lens, the ciliary body, the uvea, and the retina. The posterior cavity lies behind the lens. It is filled with a clear gelatinous substance called the vitreous humor. Vitreous humor supports the posterior surface of the lens, maintains the position of the retina, and transmits light. The lens is a biconvex, avascular, transparent structure located directly behind the pupil. It can change shape to focus and refract light onto the retina. The uvea, also called the vascular tunic, is the middle coat of the eyeball. This pigmented layer has three components: the iris, ciliary body, and choroid. The ciliary body encircles the lens, and along with the iris, regulates the amount of light reaching the retina by controlling the shape of the lens. Most of the uvea is made up of the choroids, which is pigmented and vascular. Blood vessels of the choroids nourish the other layers of the eyeball. Its pigmented areas absorb light, preventing it from scattering within the eyeball.

The retina is the innermost lining of the eyeball. It has an outer pigmented layer and an inner neural layer. The outer layer, next to the choroids, serves as the link between visual stimuli and the brain. The transparent inner layer is made up of millions of light receptors in structures called rods and cones. Rods allow for vision in dim light as well as for peripheral vision. Cones allow for vision in bright light and for the perception of color. The optic disk, a cream-colored round or oval area within the retina is the point at which the optic nerve enters the eye. The slight depression in the center of the optic disc is often called the physiologic cup. Located laterally to the optic disc is the macula, which is a darker area with no visible blood vessels. The macula contains primarily cones. The fovea centralis is a slight depression in the center of the macula that contains only cones and is a main receptor of detailed color vision THE VISUAL PATHWAY The optic nerves are cranial nerves formed of the axons of ganglion cells. The two optic nerves meet at the optic chiasma, which is just anterior to the pituitary gland in the brain. At the optic chiasma, axons from the medial half of each retina cross to the opposite side to form pairs of axons from each eye. These pairs continue as the left and right optic tracts. The crossing of the axons results in each optic tract carrying information from the lateral half of the retina of the left eye and the medial half of the retina of the right eye, whereas the right optic tract carries visual information from the lateral half of the retina of the right eye and the medial half of the retina of the left eye. The ganglion cell axons in the optic tracts travel to the thalamus and create synapses with neurons, forming pathways called optic radiation terminate in the visual cortex of the occipital lobe. Here the nerve impulses that originated in the retina are interpreted. The visual fields of each eye overlap considerably, and each eye sees a slightly different view. Because of this overlap and crossing of the axons, information from both eyes reaches each side of the visual cortex, which then fuses the information into one image. This fusion of images accounts for the ability to perceive depth; however, depth perception depends on visual input from two eyes that both focus well. Refraction Refraction is the bending of light rays as they pass from one medium to another medium of different optical density. As light rays pass through the eye, they are refracted at several points: as they enter the cornea, as they leave the cornea and enter the aqueous humor, as they enter the lens, and as they leave the lens and enter the vitreous humor. At the lens, the light is bent so that it converges at a single point on the retina. This focusing of the image is called accommodation. Because the lens is convex, the image projected onto the retina (the real image) is upside down and reversed from left to right. The real image coded as electric signals that are sent to the brain the brain decodes the image so that the person perceives it as it occurs in space. The eyes are best adapted to see distant objects. Both eyes fix on the same distant image and do not require any change in accommodation. For people with emmetropic (normal) vision, the distance from the viewed object at which the eyes require no accommodate the lens, constrict the pupils, and converge the eyeballs. Accommodation is accomplished by contraction of the ciliary muscles. This contraction reduces the tension on the lens capsule so that it bulges outward to increase the curvature. This

change in shape also achieves a shorter focal length, another requirement for the focusing of close images on the retina. The closest point on which a person can focus is called the near point of vision; in young adults with normal vision this is usually 8-10 in. pupillary constriction helps eliminate most of the divergent light rays and sharpens focus. Convergence (the medial rotation of the eyeballs so that each is directed toward the viewed object) allows the focusing of the image on the retinal fovea of each eye. Assessment of the Eyes I. Health History A. Current Health Status 1. Problems 2. Corrective lenses B. Past Health Status 1. 2. 3. 4. 5. 6. 7. 8. 9.

Lens change Blurred vision Spots, floaters, halos Infections or inflammations of the eyes Eye surgery or injury Styes (hordeolums) High blood pressure Diabetes Eye medications

C. Family health status

Equipment Needed A Snellen Eye Chart or Pocket Vision Card An Ophthalmoscope Visual Acuity In cases of eye pain, injury, or visual loss, always check visual acuity before before proceeding with the rest of the exem or putting medications in your patients eyes.

1. Allow the patient to use their glasses or contact lens if available. You are 2. 3. 4. 5.

interested in the patient's best corrected vision. Position the patient 20 feet in front of the Snellen eye chart (or hold a Rosenbaum pocket card at a 14 inch "reading" distance). Have the patient cover one eye at a time with a card. Ask the patient to read progressively smaller letters until they can go no further. Record the smallest line the patient read successfully

6. Repeat with the other eye. 7. Unexpected/unexplained loss of acuity is a sign of serious ocular pathology. Inspection 1. Observe the patient for ptosis, exophthalmos, lesions, deformities, or asymmetry. 2. Ask the patient to look up and pull down both lower eyelids to inspect the conjuntiva and sclera. 3. Next spread each eye open with your thumb and index finger. Ask the patient to look to each side and downward to expose the entire bulbar surface. 4. Note any discoloration, redness, discharge, or lesions. Note any deformity of the iris or lesion cornea. 5. If you suspect the patient has conjuntivitis, be sure to wash your hands immediately. Viral conjuntivitis is highly contagious - protect yourself! Visual Fields Screen Visual Fields by Confrontation 1. 2. 3. 4. 5. 6.

Stand two feet in front of the patient and have them look into your eyes. Hold your hands to the side half way between you and the patient. Wiggle the fingers on one hand. Ask the patient to indicate which side they see your fingers move. Repeat two or three times to test both temporal fields. If an abnormality is suspected, test the four quadrants of each eye while asking the patient to cover the opposite eye with a card.

Extraocular Muscles Corneal Reflections 1. Shine a light from directly in front of the patient. 2. The corneal reflections should be centered over the pupils. 3. Asymmetry suggests extraocular muscle pathology. Extraocular Movement 1. 2. 3. 4.

Stand or sit 3 to 6 feet in front of the patient. Ask the patient to follow your finger with their eyes without moving their head. Check gaze in the six cardinal directions using a cross or "H" pattern. Check convergence by moving your finger toward the bridge of the patient's nose.

Pupillary Reactions Light 1. Dim the room lights as necessary. 2. Ask the patient to look into the distance.

3. Shine a bright light obliquely into each pupil in turn. 4. Look for both the direct (same eye) and consensual (other eye) reactions. 5. Record pupil size in mm and any asymmetry or irregularity. Accommodation If the pupillary reactions to light are diminished or absent, check the reaction to accommodation (near reaction): [5] ++ 1. Hold your finger about 10cm from the patient's nose. 2. Ask them to alternate looking into the distance and at your finger. 3. Observe the pupillary response in each eye. Ophthalmoscopic Exam

1. Darken the room as much as possible. ++ 2. Adjust the ophthalmoscope so that the light is no brighter than necessary. Adjust the aperture to a plain white circle. Set the diopter dial to zero unless you have determined a better setting for your eyes. 3. Use your left hand and left eye to examine the patient's left eye. Use your right hand and right eye to examine the patient's right eye. Place your free hand on the patient's shoulder for better control. 4. Ask the patient to stare at a point on the wall or corner of the room. 5. Look through the ophthalmoscope and shine the light into the patient's eye from about two feet away. You should see the retina as a "red reflex." Follow the red color to move within a few inches of the patient's eye. 6. Adjust the diopter dial to bring the retina into focus. Find a blood vessel and follow it to the optic disk. Use this as a point of reference. 7. Inspect outward from the optic disk in at least four quadrants and note any abnormalities. 8. Move nasally from the disk to observe the macula. 9. Repeat for the other eye. Special Tests Upper Eyelid Eversion This procedure is performed when a foreign body is suspected. ++

1. Ask the patient to look down. 2. Gently grasp the patient's upper eyelashes and pull them out and down. 3. Place the shaft of an applicator or tongue blade about 1 cm from the lid margin. 4. Pull the lid upward using the applicator as a fulcrum to turn the lid "inside out." Do not press down on the eye itself. 5. Pin the eyelid in this position by pressing the lashes against the eyebrow while you examine the palpebral conjuntiva.

Ask the patient to blink several times to return the lid to normal.

Notes 1. Visual acuity is reported as a pair of numbers (20/20) where the first number is how far the patient is from the chart and the second number is the distance from which the "normal" eye can read a line of letters. For example, 20/40 means that at 20 feet the patient can only read letters a "normal" person can read from twice that distance. 2. You may, instead of wiggling a finger, raise one or two fingers (unialterally or bilaterally) and have the patient state how many fingers (total, both sides) they see. To test for neglect, on some trials wiggle your right and left fingers simultaneously. The patient should see movement in both hands. 3. Additional Testing - Tests marked with (++) may be skipped unless an abnormality is suspected. 4. PERRLA is a common abbreviation that stands for "Pupils Equal Round Reactive to Light and Accommodation." The use of this term is so routine that it is often used incorrectly. If you did not specifically check the accommodation reaction use the term PERRLA. Pupils with a diminished response to light but a normal response to accommodation (Argyll-Robertson Pupils) are a sign of neurosyphilis. 5. Diopters are used to measure the power of a lens. The ophthalmoscope actually has a series of small lens of different strengths on a wheel (positive diopters are labeled in green, negative in red). When you focus on the retina you "dial-in" the correct number of diopters to compensate for both the patient's and your own vision. For example, if both you and your patient wear glasses with -2 diopter correction you should expect to set the dial to -2 with your glasses on or -4 with your glasses off. DIAGNOSTIC TESTS FOR THE EYE A. FLUORESCEIN ANGIOGRAPHY It is a detailed imaging and recording of ocular circulation by a series of photographs after administration of a dye.  Preprocedure Interventions a. Assess client to allergies and previous reactions to dyes. b. Obtain informed consent c. A mydriatic medication, which causes pupil dilation, is instilled in the eye, 1 hour before the test. d. The dye is injected into a vein of the client’s arm. e. Inform the client that the dye may cause the skin to appear yellow for several hours after the test and is eliminated gradually through the urine.

f.

The client may experience nausea, vomiting, sneezing, paresthesia of the tounge or pain at the injection site.

g. If hives appear, orally or intramuscularly administered antihistamines such as diphenhydramine (Benadryl) are given as prescribed.  Postoperative Interventions a. Encourage rest. b. Encourage fluid intake to assist in eliminating the dye from the client’s system. c. Remind the client that the tallow skin appearance will disappear. d. Instruct the client that the urine will appear bright green until the dye is excreted. e. Instruct the client to avoid direct sunlight for a few hours after the test. f.

Instruct the client that the photophobia will continue until pupil size returns to normal.

B. COMPUTED TOMOGRAPHY It is a diagnostic test for the eye wherein there is a beam of x-rays scans the skull and orbits of the eye. A cross-sectional image is formed by the use of a computer and a contrast material is not usually administered.  Nursing Interventions  No special client preparation or follow- up care is required.  Instruct the client that he or she will be positioned in a confined space and will need to keep their heads still during the procedure. C. SLIT LAMP A slit lamp allows the examination of the anterior ocular structures under microscopic magnification. The client leans on a chin rest to stabilize the head while a narrowed beam of light is aimed so that it illuminates only a narrow segment of the eye.  Nursing Interventions  Explain the procedure to the client.  Advise the client about the brightness of the light and the need to look forward at a point over the examiner’s ear.

D. CORNEAL STAINING A topical dye is instilled into the conjunctival sac to outline irregularities of the corneal surface that are not easily visible. The eye is viewed to a blue filter, and a bright green color indicatesareas of a non intact corneal epithelium.  Nursing Interventions  If the client wears contact lenses, the lenses must be removed.  The client is instructed to blink after the dye has been applied to distribute the dye evenly across the cornea. E. TONOMETRY This test is used primarily to assess for an increase of intraocular pressure and potential glaucoma. Normal ocular pressure is 10- 21 mmHg.  Nursing Interventions  Each dye is anesthetized.  The client is instructed to stare forward at a point above the examiner’s ear.  A flattened cone is brought contact with the cornea.  The amount of pressure needed to flatten the cornea is measured.  The client must instructed to avoid rubbing the eye following the examination if the eye has been anesthetized because the potential for scrubbing the cornea exists. F. FUNDUS PHOTOGRAPHY

Special retinal cameras are use to document fine details of the fundus for the study and future comparison. One of the most common applications is the evaluation of insidious optic nerve changes in the clients with glaucoma. Photographs are compared over time to identify subtle changes in the clients with glaucoma. Photographs are compared over time to identify subtle changes in disc shape and color.

G. SPECULAR MIMOGRAPHY

Specular mimography is a photographic technique used to count cells of the corneal endothelium. A camera is focused on the endothelial layer, and the area is magnified 200 times; then the cell is counted. This layer of the cornea is one cell thick . cells in this layer do not reproduce but rather they expand to fill gaps in the endothelium. The number or lack of number, of cells may indicate healing potential. H. EXOPTHALMOMETRY

The exopthalmometer is an instrument designed to measure the forward protrusion of the eye. This instrument provides a method of evaluating and recording the progression and regression of the prominence of the eye in disorders such as thyroid disease and tumors of the orbit.

I.

OPTHALMIC RADIOLOGY

X-ray study, tomography, and CT scan are useful n the evaluation of orbital and intracranial conditions. Common abnormalities evaluated by these methods include neoplasms, inflammatory masses, fractures and extraocular muscle enlargement associated with Grave’s eye disease. Radiology is also useful in the detection of foreign bodies.

J. MAGNETIC RESONANCE IMAGING

MRI has the advantage of not exposing the patient to ionizing radiation. Also, multidimensional views are possible without repositioning the patient. This is used to image edema, areas of demyelination, and vascular lesions. However, the availability of MRI equipment is often lmited and the examination takes longer. MRI may also cause movement of a metallic foreign body.

K. ULTRASONOGRAPHY

Ultrasonography uses the principle of sonar to study structures not directly visible high frequency sound waves are transmitted to a probe placed directly on the eyeball. As the sound waves bounce back off the various tissue components, they are collected by a receiver that amplifies them on an oscilloscope screen. Sound waves derived from the most distal structures arrive last, having travel the farthest. Ultrasonography may be used to evaluate tissue characteristics of a lesion as well as size and growth over time. It may also be used to measure axial length (distance from the cornea to the retina) in order to calculate the power for an intraocular lens implant in cataract surgery.

L. OPTHALMODYNAMOMETRY

Opthalmodyanamometry is a test that consists of exerting pressure on the sclera with a string plunger while observing the central retinal vessels emerging from the disc through an opthalmoscope. This instrument gives an approximate measurement of the relative pressures in the central retinal arteries and is an indirect method of assessing the carotid arterial flow on either sound. M. ELECTRORETINOGRAPHY

An electrical potential exist between the cornea and retina of the eye. Because the retina is neurologic tissue, the normal retina is exhibit certain electrical responses when stimulated by light. Electroretinography (ERG) measures the normal change in electrical potential of the eye caused by a diffuse flash of light. For this test, electrodes incorporated into a contact lens are placed directly on the eye. Eye movements disrupt the values of the test, so the client must be able to fixate on a target while keeping the eyes still. A normal ERG signifies functional integrity of the retina. Examples of retinal diseases that may be th evaluated with ERG include retinitis pigmentosa (progressive degeneration of photoreceptor cells), massive ischemia, disseminated infection, or toxic effects from drugs or chemicals. N. VISUAL EVOKED RESPONSE

Visual evoked response (VER) is similar to ERG in that it also measures the electrical potential resulting from a visual stimulus. The entire visual pathway

from the retina to the cortex maybe evaluated in the examination through the placement of electrodes on the scalp. Reduces speed of neuronal conduction, such as with demyelination, results in an abnormal VER. Retina or optic nerve disease may be diagnosed by stimulating each eye separately.

EYE DISORDERS Degenerative Disorders A. GLAUCOMA Glaucoma includes a group of ocular disorders characterized by increase intraocular pressure, optic nerve atrophy and visual field loss. The individual response to intraocular pressure varies. Therefore, some people sustain damage from relatively low pressures and others sustain no damage from high pressure. The degree of increase pressure that cause ocular damage is not the same in every eye, and some individuals may tolerate a pressure for long periods of time that would rapidly blind another. •

Incidence

It is estimated that over 50,000 persons in the US are blind as a result of glaucoma. The incidence of glaucoma is about 1.5%, and in blacks, between the ages of 45 and 65, prevalence is at least five times that of the whites in the same age group. In most cases, blindeness can be prevented if treatment is began early. Glaucoma is called the “sneak thief of sight” because it strikes without obvious symptoms. People with glaucoma are usually unaware of it until they have a serious loss of vision. In fact, about half of those who have glaucoma do not know it. Currently, that damage cannot be reversed. While there are usually no warning signs, some symptoms may occur in the later stages of the disease, such as a loss of peripheral vision, difficulty focusing on close work, seeing halos around lights, and frequent changes of prescription glasses. Unfortunately, though, once the vision is lost, it is gone forever. African Americans are at a higher risk of developing glaucoma than other racial groups. Others at risk include: • • • •

•

Anyone with a close relative who has glaucoma; Seniors; People with diabetes; People taking steroid medications for extended periods of time. Pathophysiology

Intraocular pressure is determined by the rate of aqueous production in the cilliary body and the resistance to outflow aqueous from the eye. Increase intraocular pressure (usually greater that 23mm Hg) indicates the need for further evaluation.

Intraocular pressure varies with diurnal cycles. (the highest pressure is usually on awakening) and position of the body (increase when lying down). Normal variation do not usually exceed 2-3 mm Hg. Intraocular pressure and blood pressure are independent of each pther but variations in the systemic blood pressure may be associate with corresponding variations in the intraocular pressures. Increase intraocular pressure may result from hyper production of aqueous or obstruction of the outflow. As aqueous fluid builds up in the eye, the increase pressure inhibits blood supply to the optic nerve and the retina. These delicate tissues become ischemic and gradually loss function. • Etiology/ Risk Factors Many terms are used to describe the various types of glaucoma. The terms primary and secondary refer to whether the etiology is the disease alone or due to another condition. Acute and chronic refer to the onset and/ duration of the disorder. The terms open (wide) and closed (narrow) describe the width of the ngle between the cornea and the iris. Anatomically narrow anterior chamber angles predispose clients to an acute onset of angle-closure glaucoma. TYPES OF GLAUCOMA  Primary Open-Angle Glaucoma Approximately 90% of primary glaucoma cases occur in clients with open angles. It is a multifunctional disorder that is often genetically determined, bilateral, ininsidious in onset, and slow to progress. Symptoms appear late when vision is impaired by damage to the optic nerve. Because there are no early warning symptoms, it is imperative that regular ophthalmic examinations include tonometry and assessment the optic nerve head (disc). This type of glaucoma is often referred t as the “THIEF IN THE NIGHT” because there are no early symptoms alerting the client that vision is being lost. The most common cause of chronic open angle glaucoma is degenerative change in the trabecular meshwork, resulting in the decrease outflow of aqueous humor.  Angle- Closure Glaucoma An acute attack of angle-closure glaucoma can develop only in an eye in which the anterior chamber angle is anatomically narrow. The attack occurs due to a sudden blockage of an anterior angle by the base of the iris. When the aqueous flow is obstructed, intraocular pressure becomes markedly elevated, causing severe pain and blurred vision or vision loss. Some client will see rainbow halos around lights, and some will experience nausea and vomiting.  Low Tension Glaucoma Low-tension glaucoma resembles primary open-angle glaucoma. The angle is normal, the optic nerves are cupped and the visual fields show characteristic glaucomatous effects. (peripheral vision deficits). These changes, however, develop in the presence statistically normal intraocular pressures. The etiology of low tensions glaucoma is not known. Although the pressure readings are in the normal range, treatment is indicated to lower the pressure even further to avoid progressive optic nerve damage and visual field loss.  Secondary Glaucoma

Increase intraocular pressure may occur as a post operative complication. Edematous tissue may inhibit the outflow of aqueous through the trabecular meshwork. Delayed healing of corneal would edges may result in epithelial cell growth into the anterior chamber. Glaucoma may occur as a result of trauma. Lens displacement, hemorrhage into the anterior chamber, laceration, and contusions can dirupt the flow pattern of aqueous humor. • Clinical Manifestations Clinical manifestations of glaucoma include: 1. Increase intraocular pressure, 2. Cupping or indentation of the optic nerve head (disc) and 3. Visual field defects

•

Diagnostic Assessment

An opthalmoscopic examination shows atrophy (pale color) and cupping (indentation) of the optic nerve head. The visual field examination is used to determine the extent of peripheral vision loss (see the section on visual fields). In chronic open angle glaucoma, a small crescent- shape scotoma (blind spot) appears early in the disease. In acute angle-closure glaucoma, the fields demonstrate larger areas significant vision loss. In clients with angle-closure glaucoma, a slit lamp examination may demonstrate an erythematous conjunctiva and corneal cloudiness. The anterior chamber aqueous may also appear turbid and the pupil may be non reactive. Slit lamp examination is used in open angle glaucoma to look for any secondary causes and associate findings. Intraocular pressure is measured at the slit lamp with the applanation tonometer. Gonioscopy is performed to determine the depth of the anterior chamber and to examine the entire circumference of the angle for any abnormal change in the filtering meshwork. • Medical Management The goal of medical management is to facilitate the outflow of aqueous through remaining channels. This is achieved through the use of  Topical miotics, which constricts the pupil and increase outflow ;  Topical epinephrine, which also increase the outflow;  Topical beta blockers or alpha adrenergics, which suppress the secretion of aqueous humor; and  Oral carbonic anhydrase inhibitors, which also reduce the production of aqueous humor. When mediacal management is no longer effective, surgical intervention may be indicated. • Surgical Management

When maximum medical therapy has failed to halt the progression of visual field loss and optic nerve damage, surgical intervention is recommended. There are many procedures that are use to correct the aqueous outflow; however, there is no operation that is uniformly successful. •

Laser Trabeculocospy

The use of laser to create an opening in the trabecular meshwork is often indicated before filtration surgery is considered. The laser produces scars in the trabecular meshwork fibers. The tightened fibers allow increased outflow of aqueous. Intraocular pressure is reduced through improved outflow in about 80% of cases. • Filtering Procedures Operative procedures such as trephination, thermal sclerostomy, or scleroctomy create an outflow channel from the anterior chamber to the subconjunctival space. These are called filtering procedures. Aqueous is absorbed through the conjunctival vessels. In about 25% of cases, the opening closes due to scar tissue formation, and reoperation is necessary. • Ciliodestructive Procedures When other surgical procedures have failed, cyclocryotherapy (application of freezing tip) or cyclophotocoagulation may be used to damage the ciliary body and decrease the production of aqueous. •

ASSESSMENT

 Progressive loss of peripheral vision followed by loss of central vision  Elevated intraocular pressure (normal pressure is 10- 21 mmHg)  Vision worsening in the evening with difficulty adjusting to dark rooms  Blurred vision  Halos around white lights  Frontal headaches  Eye pain  Photophobia  Lacrimation  Progressive loss of central vision •

NURSING INTERVENTIONS

Acute Glaucoma  Administer medications s prescribe to lower intraocular pressure. And prepare the client for peripheral indectomy, which allows aqueous humor to flow from the posterior to anterior chamber. Chronic Glaucoma  Instruct the client on the importance of medications (miotics) to constrict the pupils, (carbonic anhydrase inhibitors) to decrease production of aqueous humor, and beta blockers to decrease the production of aqueous humor and intraocular pressure.  Instruct the client on the need for lifelong medication use and to avoid anticholinergic medications.  Instruct the client to report eye pain, halos around the eyes, and changes in vision to the physician.  Teach the client that when maximal medical therapy has failed to halt the progression of visual field loss and optic nerve damage, surgery will be recommended.  Prepare the client for trabeculoplasty as prescribed to facilitate aqueous humor drainage and to allow drainage of aqueous humor into the conjunctival spaces b the creation of an opening.

B. CATARACT

•

Definition

A cataract is a cloudy or opaque area (an area you cannot see through) in the lens of the eye. It is an opacity of the lens that distorts the image projected onto the retina and that can progress to blindness. •

Alternative Names

Lens opacity •

Causes, incidence, and risk factors

The lens of the eye is normally clear. If the lens becomes cloudy, the condition is known as a cataract. Rarely, cataracts may be present at or shortly after birth. These are called congenital cataracts.

Adult cataracts usually develop with advancing age and may run in families. Cataracts develop more quickly in the presence of some environmental factors, such as smoking or exposure to other toxic substances. They may develop at any time after an eye injury. Metabolic diseases such as diabetes also greatly increase the risk for cataracts. Certain medications, such as cortisone, can also accelerate cataract formation. Congenital cataracts may be inherited. The gene for such cataracts is dominant (autosomal dominant inheritance), which means that the defective gene will cause the condition even if only one parent passes it along. I families where one parent carries the gene, there is a 50% chance in every pregnancy that the child will be affected. Congenital cataracts can also be caused by infections affecting the mother during pregnancy, such as rubella. They are also associated with metabolic disorders such as galactosemia. Risk factors include inherited metabolic diseases, a family history of cataracts, and maternal viral infection during pregnancy. Adult cataracts are generally associated with aging. They develop slowly and painlessly, and vision in the affected eye or eyes slowly gets worse. Visual problems may include the following changes: • • •

Difficulty seeing at night Seeing halos around lights Being sensitive to glare

Vision problems associated with cataracts generally move towards decreased vision, even in daylight. Adult cataracts are classified as immature, mature, and hypermature. A lens that has some remaining clear areas is referred to as an immature cataract. A mature cataract is completely opaque. A hypermature cataract has a liquefied surface that leaks through the capsule, and may cause swelling and irritation of other structures in the eye. Most people develop some clouding of the lens after the age of 60. About 50% of people aged 65-74, and about 70% of those 75 and older, have cataracts that affect their vision. Most people with cataracts have similar changes in both eyes, although one eye may be worse than the other. Many people with this condition have only slight visual changes, and are not aware of their cataracts. Factors that may contribute to cataract development are low serum calcium levels, diabetes, long-term use of corticosteroids, and various inflammatory and metabolic disorders. Environmental causes include trauma, radiation exposure, and too much exposure to ultraviolet light (sunlight). •

Symptoms • Cloudy, fuzzy, foggy, or filmy vision

• • • • • • •

• • •

Loss of color intensity Frequent changes in eyeglass prescription The glare from bright lights causes vision problems at night, especially while driving Sensitivity to glare from lamps or the sun Halos around lights Double vision in one eye Decreased contrast sensitivity (the ability to see shades, or shapes against a background) Signs and tests Standard ophthalmic exam, including slit lamp examination Ultrasonography of the eye in preparation for cataract surgery

Other tests that may be done (rarely) include: • • • •

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Glare test Contrast sensitivity test Potential vision test Specular microscopy of the cornea in preparation for cataract surgery Treatment

The only treatment for cataract is surgery to remove it. This is done when a person cannot perform normal activities, even with glasses. For some people, changing glasses, getting stronger bifocals, or using a magnifying lens is helpful enough. Others choose to have cataract surgery. If a cataract is not bothersome, then surgery is usually not necessary. Sometimes there is an additional eye problem that cannot be treated without first having cataract surgery. Cataract surgery consists of removing the lens of the eye and replacing it with an artificial lens. A cataract surgeon will discuss the options with the patient, and together they will decide which type of removal and lens replacement is best. •

LENS REMOVAL:

There are 2 types of surgery that can be used to remove lenses that have a cataract. Extracapsular surgery consists of surgically removing the lens, but leaving the back half of the capsule (the outer covering of the lens) whole. High-frequency sound waves (phacoemulsification) may be used to soften the lens to help removing it through a smaller cut. With extracapsular extraction, the lens is lifted out without removing the lens capsule; the procedure may be performed by phacoemulsification in which the lens is broken up by ultrasonic vibrations and is extracted. Intracapsular surgery involves surgically removing the entire lens, including the capsule. Today this procedure is done very rarely. In this procedure, lens is removed within capsule through a small incision.

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LENS REPLACEMENT:

People who have cataract surgery are usually fitted with an artificial lens at the same time. The artificial lens is a synthetic (manufactured) disc called an intraocular lens. It is usually placed in the lens capsule inside the eye. Other options include contact lenses and cataract glasses. Surgery can be done in an outpatient center or hospital. Most people do not need to stay overnight in a hospital. The patient will need a friend or family member to assist with travel and home care after outpatient surgery. Follow-up care by the surgeon is important. •

NURSING INTERVENTIONS

Preoperative Interventions  Instruct the client regarding the postoperative measures to prevent or decrease intraocular pressure.  Administer eye medications preoperatively, including mydriatics and cycloplegics as prescribed. Postoperative Interventions      

Elevate the head of the bed 30- 45 degrees. Turn the client to the back or unoperative side Maintain an eye patch; orient the client to the environment Position the client’s personal belongings to the unoperative side Use side rails for safety Assist with ambulation

AGE RELATED MACULAR DEGENERATION Previously known as the senile macular degeneration, age related macular degeneration is an atrophic degenerative process that affects the macula and surrounding tissues, resulting in central visual deficits. Age related macular degeneration can be found in some degree to some adults over the age of 65. It is one of the most common causes of visual loss in the elderly. The exact etiology is unknown, but the incidence increases with each decade over 50. It may also be hereditary. Age- related macular degeneration falls into two categories: 1. Nonexudative 2. Exudative Both are usually bilateral and progressive.

Also referred to as “dry” macular degeneration, nonexudative age related macular degeneration is characterized by atrophy and degeneration of the outer retina and underlying structures. Yellowish round spots called drusen may be seen in the retina and macula with an opthalmoscope. Drusen are deposits of amorphous material from the pigment epithelial cells of the retina. Overtime, these spots increase, enlarge and may calcify. At this, “wet”, exudative stage of age-related macular degeneration, Bruch’s membrane, which lies just beneath the pigment epithelial cell layer of the retina, becomes compromised and this results in serous fluid leaks from the colloid with accompanying proliferation of choroidal blood vessels. A dome-shaped retinal pigment epithelium may be seen when examining the fundus. These leak produce a visual effect called tamorphopsia, which is the blurred, wavy distortion vision. The client may also notice blurred scotomo or decrease central visual acuity. Fundus photograpghy and angiography may be performed on a regular basis of documents and evaluate changes. •

Management

There is no known means of medical treatment or prevention for age elated macular degeneration. Further damage from exudative macular degeneration sometimes may be arrested by the use of argon photocoagulation, even though laser bamage to the retina in this area results in a blind spot. When the fovea is involved, central vision is lost and he only helpful measures are low-vision aids. The client with age-related macular degeneration is threatened with the loss of central vision. In order to evaluate change in vision, the client is taught to use an Amsler grid at home. The nurse may be able to assist the client to maximize remaining vision with low vision aids and community referral to a low vision specialist and low vision support groups. C. RETINAL DETACHMENT Retinal detachment occurs when the layers of the retina separate because of the accumulation of fluid between them, or when both retinal layers elevate away from the choroid as a result of a tumor. Partial separation becomes complete if untreated. When detachment becomes complete, blindness occurs. • Assessment

 Flashes of lights  Floaters  Increase in blurred vision  Sense of curtain being drawn  Loss of a portion of the visual field •

Immediate Interventions

 Provide bed rest  Cover both eyes with patches to prevent further detachment  Speak to the client before approaching  Position the client head as prescribed  Protect the client from injury  Avoid jerky head movements  Minimize eye stress  Prepare the client for the surgical procedure as prescribed. Surgical Procedures • Draining fluid from the subretinal space so that the retina can return to the normal position. •

Sealing retinal breaks by cryosurgery, a cold probe applied to the sclera, to stimulate an inflammatory response leading to adhesions.

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Diathermy, the use of an electrode needle and heat through the sclera, to stimulate an inflammatory response.

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Laser therapy to stimulate an inflammatory response, to seal small retinal tears before the detachment occurs.

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Sclera buckling, to hold the choroid and retina together with a splint until scar tissue forms closing the tear.

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Insertion of gas or silicon oil to encourage attachment because these agents have a specific gravity less than vitreous or air and can float against the retina. •

Postoperative Interventions

 Maintain eye patches bilaterally as prescribed.  Monitor for hemorrhage.  Prevent nausea and vomiting and monitor for restlessness, which can cause hemorrhage.  Monitor for sudden sharp eye pain and monitor the physician.

 Encourage deep breathing exercise but avoid coughing.  Provide bed rest for 1-2 days and position the client as prescribed.  If gas has been inserted, position the client as prescribed on the abdomen and turn the head so unaffected eye is down.  Administer eye medications as prescribed.  Assist the client with activities of daily living.  Avoid sudden head movements or anything that increases intraocular pressure.  Instruct the client to limit reading for 3-5 weeks.  Instruct the client to avoid squinting, straining and constipation, lifting heavy objects and bending from the waist.  Instruct the client to wear dark glasses during the day and an eye patch at night.  Encourage follow-up care because of the danger of recurrence in the other eye. REFRACTIVE DISORDERS Light is bent (refracted) as it passes through the cornea and lens of the eye. Refractive errors exist when light rays are not focused appropriately on the retina of the eye. Three basic abnormalities of refraction occur in the eye: 1) myopia 2) hyperopia, and 3) astigmatism. Optical correction is important to distinguish between visual loss caused by disease and visual loss caused by refractive error. Refractometry is the measurement of refractive error and should not be confused with refraction, the method used to determine which lens or lenses (if any) will most benefit the client.

a. Myopia Myopia, or nearsightedness, is a condition in which the light rays come into focus in front of the retina. In this case the refractive power of the eye is too strong and a concave, or minus, lens is used to focus light rays on the ey. In most cases myopia is caused by an eyeball that is longer than normal, which may be a familial triat. Transient myopia may occur with the administration of a variety of medications (sulfonamides, acetozolamide, salicylates, and steroids) and has been associated with other disorders,

such as influenza, typhoid fever, severe dehydration, and large intakes of antacids. Correction is accomplished with eyeglasses or contact lenses. b. Hyperopia The hyperopic, or farsighted, eye focuses light rays behind the eye, and consequently the image that falls on the retina is blurred. Vision may be brought into focus by placing a convex, or plus, lens in front of the eye. The lens supplies the magnifying power that the eye is lacking. Hyperopia may be caused by an eyeball that is shorter than normal or a cornea that has less curvature than normal. Because children have a greater ability to accommodate, they are less often affected than adults. Demands for close work and reading usually bring on manifestations of headache or eye strain. Correction is based on a person’s age and individual needs and complaints. c. Astigmatism Astigmatism is a refractive condition in which rays of light are not bent equally by the cornea in all direction so that a point of focus is not attained. In most instances, astigmatism is caused because the curvature of the cornea is not perfectly spherical. This is the cause of poor vision for both distant and near objects. Astigmatism is corrected with cylindrical lenses.

Surgical management The following are the three main types of refractive surgery and new procedure.

Laser in situ keratomileusis (LASIK) is currently the most commonly used corrective surgery for nearsightedness in the United States. An extremely thin layer of the cornea is peeled back for the laser reshaping on the middle layer of the cornea and then put back in place. There is little postoperative discomfort, rapid recovery of clear vision, and quick stabilization of refractive change. LASIK is performed in a surgeon’s office or samedday surgery center and does not require a hospital stay. It takes about 10-15 minutes per eye. It has a high success rate and low complication rate for low to moderate nearsightedness and may also be used to correct more severe nearsightedness.

Excimer laser photorefractive keratectomy (PRK) uses short-wavelenght, high-energy ultraviolet radiation laser to reshape the corneal surface. In PRK for myopia, the central cornea is flattened with the excimer laser. The same laser may be used to reshape the cornea by making the central curvature steeper to correct hyperopia. It may be used to correct nearsightedness and astigmatism at the same time. PRK is performed on an outpatient basis in a surgeon’s office or same-day surgery center. The PRK procedure takes about 30 minutes, most of which is spent teaching the client to hold the eye still. The actual treatment takes less than a minute. Recovery from PRK is longer and more painful than recovery from ether radial keratotomy (RK) or LASIK. Vision will be reduced for several days after surgery.

Radial keratotomy (RK) involves making tiny cuts in the cornea, which flatten it and reduce nearsightedness. In people who have both astigmatism and nearsightedness, the surgeon may make additional cutrs to flatten the misshapen part of the cornea that is causing the astigmatism. RK is an outpatient procedure. It is done under local or topical anesthesia in a surgeon’s office or same day surgery center.

Corneal ring implants are clear pieces of acrytic that can be surgically implanted into the cornea. The implants are shaped like crescents or half circles. Two implants are used for each eye, and the implants are inserted along the sides of the cornea. Nursing management of the surgical client Clients are assessed preoperatively for degree of myopia or astigmatism. Clients with a severe case usually cannot achieve full correction. Surgery is performed on an out patient basis with local anesthesia. Eye protection is used, such as goggles to prevent dry eyes. Vigorous activities, activities that cold get water in the eye, and eye makeup are to be avoided. The eye is treated with steroid eyed drops, and most clients report watering of the eyes and minimal pain. Refraction slowly stabilizes after surgery. There is a period of adjustment during which visual acuity waxes and wanes. Reduced contrast sensitivity in night vision and daytime glare is common. Some clients require re treatment for scarring that is unresponsive to topical steroids.

Infectious and Inflammatory Conditions Inflammation and infection of eye structures are common. Eye infection is a leading cause of blindness worldwide. • Dry eye syndrome Dry eye syndrome, or keratoconjuctivitis sicca, is a deficiency in the production of any of the aquaeous, mucin, or lipid tear film components; lid surface abnormalities; or epithelial abnormalities related to systemic diseases (eg, thyroid disorders, Parkinson’s

disease), infection, injury, or complications of medications (eg. Antihistamines, oral contraceptives, phenothiazines) Clinical manifestations The most common complaint in dry eye syndrome is a scratchy or foreign body sensation. Other symptoms include itching, excessive mucus secretions, inability to produce tears, a burning sensation, redness, pain, and difficulty moving the lids. Assessment and diagnostic findings Slit-lamp examination shows an absent or interrupted tear meniscus at the lower lid margin, and the conjuctiva is thickened, edematous, and hyperemic and has lost its luster. A tear meniscus is the crescent-shaped edge of the tear film in the lower lid margin. Chronic dry eyes may result in chronic conjuctival and corneal irritation that can lead to corneal erosion, scarring, ulceration, thinning, or perforation that can seriously threaten vision. Secondary bacterial infection can occur. Management Management of dry eye syndrome requires the complete cooperation of the patient with a regimen that needs to be followed at home for a long period; otherwise, complete relief of symptoms is unlikely. Instillation of artificial tears during the day and an ointment at night is the usual regimen to hydrate and lubricate the eye and preserve a moist ocular surface. Anti-inflammatory medications are also used, and moisture chambers (eg, moisture chamber spectacles, swim goggles) may provide additional relief. Patients may become hypersensitive to chemical preservatives such as benzalkonium chloride and themerosal. For these patients, preservative-free ophthalmic solutions are used. Management of the dry eye syndrome also includes the concurrent treatment of infections such as chronic blepharitis and acne rasacea, and treating the underlying systemic disease. • Conjunctivitis Conjunctivitis (inflammation of the conjuctiva) is the most common ocular disease worldwide. It is characterized by a pink appearance (hence the common term pink eye) because of subconjuctival blood vessel congestion. Clinical manifestations General symptoms include foreign body sensation, scratching or burning sensation, itching, and photophobia. Conjunctivitis may be unilateral or bilateral, but the infection usually starts in one eye and then spreads to the other eye by hand contact. Assessment and Diagnostic Findings The four main clinical features important to evaluate are the type of discharge (watery, mucoid, purulent, or mucopurulent), type of conjuctival reaction (follicular or papillary), presence of pseudomembranes or true membranes, and presence or absence of lymphadenopathy (enlargement of the preauricular and submandibular lymph nodes where the eyelids drain). Pseudomembranes consist of coagulated exudates that adheres to the surface to the superficial layer of the ocnjuctiva, and moval results in bleeding. Follicles are multiple, slightly elevated lesions encircled by tiny blood vessels; they look like grains of rice. Papillae are hyperplastic conjuctival epithelium in numerous projections that are usually seen as a fine mosaic pattern under slit-lamp examination. Diagnosis is based on the distinctive characteristics of ocular signs, acute or chronic

presentation, and identification of any precipitating events. smear preparations and cutures confirm the diagnosis

Positive results of swab

Types of conjunctivitis: 1. Microbial conjunctivitis Bacterial conjunctivitis can be acute or chronic. The acute type can develop into a chronic condition. Signs and symptoms can vary from mild to severe. Chronic bacterial conjunctivitis is usually seen in patients with lacrimal duct obstruction, chronic dacryocystitis, and chronic blepharitis. The most common causative microorganisms are streptococcus pneumoniae, haemophilus influenzae, and staphylococcus aureaus. It is manifested with an acute onset of redness, burning, and discharge. 2. Viral conjunctivitis Viral conjunctivitis can be acute and chronic. The discharge is watery, and follicles are prominent. Severe cases include psudomemebranes. The common causative organisms are adenovirus and herpes simplex virus. Conjunctivitis caused by adenovirus is highly contagious. The condition isusually preceded by symptoms of upper respiratory infection. Corneal involvement causes extreme photophobia. Symptoms include extreme tearing, redness, and foreign body sensation that can involve one or both eyes. There is lid edema, ptosis, and conjuctiva hyperemia (dilation of the conjuctival blood vessels). These signs and symptoms vary from mild to sever and may last for 2 weeks. 3. Allergic conjunctivitis Immunologic or allergic conjunctivitis is a hypersensitivity reaction that occurs as part of allergic rhinitis (hay fever), or it can be an independent allergic reaction. The patient usually has a history of an allergy to pollens and other environmental allergens. There is extreme pruritus, epiphora (excessive secretion of tears), injection, and usually severe photophobia.

4. Toxic conjunctivitis Chemical conjunctivitis can be the result of medications; chlorine from swimming pools; exposure to toxic fumes among industrial workers; or exposure to other irritants such as smoke, hair sprays, acids, and alkalis. Management The management of conjunctivitis depends on the type. Most types of mild and viral conjuctivits are self-limiting, benign conditions that may not require treatment and laboratory procedures. For more severe cases, topical antibiotic therapy, eye drops, or ointments are prescribed. Patients with gonococcal conjunctivitis require urgent antibiotic therapy. If left untreated, this ocular disease can lead to corneal perforation and blindness. The systemic complications can include meningitis and generalized septicemia. • UVIEITIS Inflammation of the uveal tract (uveitis) can affect the iris, the ciliary body, or the choroids. There are two types of uveitis: nongranulomatous and granulomatous. The more common type of uveitis is the nongranulomatous type, which manifests as an acute condition with pain, photophobia, and a pattern of conjuctival injection, especially around the cornea. The pupil is small or irregular, and vision is blurred. There may be small, fine precipitates on the posterior corneal surface and cells in the aqueous humor.

If the uveitis is severe, a hypopyon (accutmulation of pus in the anterior chamber) may occur. The condition may be unilateral or bilateral and may be recurrent. Management Because photophobia is a common symptom, patients should wear dark glasses outdoors. Ciliary spasm and synechia are best avoided through mydriasis; cyclopentolate and atropine are commonly used. Local corticosteroid drops such as Pred Forte 1% and Flarex 0.1%, instilled four to six times a day are also used to decrease inflammation. In very severe cases, systemic corticosteroids as well as intravitreal corticosteroids, may be used.

DISORDER OF THE AUDITORY SYSTEM Ear disease causes significant discomfort and hearing loss. It also creates work loss and decreased productivity-- this increases as the persons communicative skills decrease when associated hearing loss increases. In children, developmental delays and academic failure my result due to manifestation of auditory problem if not properly treated. Ear Complications such as deafness, meningitis, brain abscesses, and facial nerve paralysis may also occur. Proper management of ear disease is critical and immediate attention is necessary.

COMMON DISEASES AND DISORDER OF THE MIDDLE EAR

 Otitis Media (Middle Ear Infections) The basic underlying problem causing most forms of otitis is eustachian tube dysfunction. Most otitis occurs in patients whose eustachian tube, the tube between the nose and the middle ear the area behind the eardrum, does not work properly. When air cannot adequately get through this tube to the middle ear, the negative pressure created can "suck" fluid out of the lining of the middle ear/mastoid, filling the middle ear and mastoid air cells with fluid. A mild hearing loss usually accompanies the fluid. The hearing loss disappears when the fluid is gone as long as there are no other causes for the hearing loss. Three kinds of otitis can result from eustachian tube dysfunction. They are serous and secretory otitis, where fluid fills the middle ear and mastoid, acute otitis, where pus fills the middle ear and mastoid but its presence is of short duration, and chronic otitis, where pus fills the middle ear and mastoid and it has been present for months or years. Chronic otitis is associated with infection of the bone itself and thickening and polyp formation of the mucosal lining of the middle ear and mastoid. The highest incidence of otitis media occurs in preschool children and decreases gradually after age 6. The highest incidence occurs poor children, children in day care, and Native Americans. Additional factors that cause or aggravate otitis include the presence of enlarged adenoid tissue, lack of proper muscle in the back of the throat (as in those with a cleft palate), allergy, immune deficiencies, sudden change in atmospheric pressure (like poor pressurization in an airplane dropping from a high altitude), scarring or tumors in the nasopharynx, and abnormal cell function of the mucosa of the ear and nose. Diabetes does not increase the incidence of otitis, but can make it much more difficult to treat. Types of Otitis Media

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Serous otitis- where fairly clear fluid fills the middle ear and mastoid occurs with fairly sudden obstruction of the eustachian tube. A sudden descent of an airplane with poor pressurization or a bad cold are two of the most common causes of

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acute serous otitis media. Usually decongestants will clear the fluid or even bloods that can be sucked from the mucosa into the middle ear with wither of these processes. If the fluid does not clear within a few weeks, it is considered chronic serous otitis. Older people with poorly functioning eustachian tubes commonly have recurrent serous otitis and may require intermittent tube placement over many years. Hearing loss is present depending on the amount of fluid in the ear. The hearing loss usually resolves when the fluid is cleared out of the ear, either medically or surgically. Secretory otitis- where somewhat thicker fluid fills the middle ear and mastoid is common in small children and is often "outgrown" by the time they reach their teens. It is the most common disease process requiring the placement of PE tubes. This thicker fluid has components that are actually "secreted" by the mucous glands of the middle ear. There are actually tissue breakdown enzymes in this fluid; that, if left untreated, can gradually eat away bone and cause chronic hearing loss/damage. Luckily, it generally takes quite a while for these enzymes to cause damage to the ear, so treating secretory otitis in children with medication for a few weeks or months is safe. Leaving this kind of fluid in an ear for more than several months, however, places the ear tissues (including the tiny ear bones) at risk of damage or destruction by these enzymes. Not treating infections with antibiotics at all places the ear structure at even higher risk of permanent damage/destruction by the fluid. Acute otitis- occurs when pus fills the middle ear. It is usually sudden in onset and is often associated with sudden obstruction of the eustachian tube at the same time infections bacteria are present to cause the acute otitis. Without antibiotic treatment, a true bacterial acute otitis is often associated with sudden perforation of the eardrum, with profuse drainage from the ear. Often the eardrum will spontaneously heal over after the infection has resolved, but a perforation can be left and damage to the middle ear and/or the inner ear can accompany the infection. The eardrum may be bright red or the creamy color of the fluid can sometimes be seen through the eardrum. It sometimes looks "soggy." Pain and fever may accompany an ear infection, but usually disappear rapidly if the eardrum perforates. Pain and fever are rarely present if there is a whole (perforation) in the eardrum before the infection starts. The standard treatment of acute otitis media is oral antibiotics. Ear drops are added if the eardrum perforates. IV antibiotics are indicated for severe infections, if the mastoid bone is also infected, or if the facial nerve becomes paralyzed as a "complication" of the acute infections. Hearing loss is present but usually goes away when the infection clears. Chronic otitis-occurs when chronic infection fills the middle ear space and mastoid cavity. True chronic otitis media is almost always a form of chronic mastoiditis, where the bone of the mastoid cavity (the honeycombed bone behind the ear) is chronically infected along with the tissues of the middle ear space. It is important to realize that antibiotics alone usually cannot remove infection from the bone; surgical removal of the infected bone is usually necessary to accomplish this. Even IV antibiotics do not often eradicate a true bone infection, especially in the mastoid, which has its connection to the bacteria-filled nose through the eustachian tube. A cholesteatoma is a common additional finding along with chronic otitis and mastoiditis. A cholesteatoma is a skin sac that grows back into the middle ear or mastoid from the eardrum, creating a mass of skin and debris that keeps getting larger and larger over time, destroying anything in

its path. The ear bones, the inner ear, the facial nerve (the nerve that makes all the muscles of one side of your face work), and the brain next to the ear can all be damaged or destroyed by either spreading infection or cholesteatoma. These diseases must be removed fore the safety of the ear, the head, and the brain. Infection or cholesteatoma involving the inner ear, facial nerve, or the brain requires immediate attention by an ear surgeon and often required immediate surgery. Symptoms of Middle Ear Infection • • • • • • •

Earache Headache Fever Discharge from the ear Mild deafness Difficulties in sleeping Loss of appetite.

The causes of middle ear infection: • • • • •

A progressive head cold A viral sinus infection that spreads An otitis externa infection left too long that spreads to the inner ear Blowing the nose too hard, forcing sinal or eustachian material into the middle ear. An opportunistic infection entering through a perforated eardrum

Treatments for Otitis Media Mild bacterial infections often clear up by themselves in a matter of days. Overthe-counter painkillers can help alleviate the pain. Warm olive oil dripped in the ear can also soothe the pain as long as there is no ruptured eardrum. Repeat every few hours. In more severe cases, antibiotics might be needed which usually includes an initial antibiotic shot, antibiotic pills and ear drops. In many cases of middle ear infection, the Eustachian tube is blocked and can cause or at least contributes to a middle ear infection. A Eustachian tube can become blocked from any combination of the following: •

The body's inflammation reaction to an infection, swelling the Eustachian tube to where it closes completely.

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A contributing factor can be the discharge of the dead bacteria and dead lymphocytes from the middle ear. The lymphatic system contains the white blood cells or lymphocytes which are the body's defense against foreign objects such as bacteria. When the white blood cells kill bacteria, the lymphatic fluid becomes pus-like due to a build up of dead white blood cells

and dead bacteria. This discharge from the middle ear can irritate the Eustachian tube causing it to close. A blocked Eustachian tube is often what causes the pain of a middle ear infection. Pus builds up in the inner ear cavity with no where to go, putting pressure on the inner ear and the ear drum. If left without treatment, the pressure can be so great that it bursts the ear drum. The initial excruciating pain of a burst eardrum is immediately compensated for by pain reduction from the release of pressure. Whereas, prior to the burst eardrum, sleep was impossible, the pain relief from the pressure reduction allows the sufferer to finally sleep. If the middle ear infection is cured on its own, the ruptured ear drum will also usually heal on its own, although sometimes surgery (tympanoplasty) is indicated if the rupture is extremely large.

 Chronic Suppurative Otitis Media (CSOM) CSOM is the name given to a condition when there is an infection of the middle ear which fails to heal and is draining all the time.

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Glue Ear

There is a natural flow of fluids from the middle ear (the fluids keep the middle ear cavity moist) that migrate through the Eustachian tube to the back of the throat. A blocked Eustachian tube prevents air from reaching the middle ear. When this happens the middle ear can fill up with the fluid that can becomes thick, like glue over time. This problem is called glue ear or otitis media with effusion. The buildup of fluid in the middle ear reduces the movement of the eardrum and ossicles, and hearing is reduced. This condition is quite prevalent in children. Glue Ear is not a disorder in itself, it is just a visible symptom of a discharge of bacterial waste from the middle ear. Note: Glue ear is sometimes confused by anxious parents with the normal discharge of wax from a child's ear canal. During an infant or child's growth, there may be periods when ear wax is produced more copiously than normal, causing wax to leak from the ear. How to tell the difference: • •

If the child has not had a fever then it is a normal wax discharge If the child has not complained of earache then it is a normal wax discharge

If the discharge does not have a really smelly odor then it is a normal wax discharge (there is a slight odor to normal wax, but nothing like that from waste bacteria from the middle ear) Predisposition factors for Otitis Media and Glue Ear There are factors that can increase the risk of a child being susceptible to otitis media and glue ear:

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being a male short length of breastfeeding attendance at day care centers parental smoking wet climate winter season upper respiratory infection housing with mold allergies

Symptoms of Glue Ear

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A thick liquid discharge from the ear that looks like liquid wax and is orange in color. Ear aches Headaches Fever Listlessness They may be clumsy. With very small infants (1-3 years old), it might also take them longer to start to walk, speak or understand language. Older children may be able to tell you if they cannot hear very well. Or you may notice that they say 'pardon' or 'what' a lot or that they turn the television up loud. Glue ear also makes older children clumsy and dizzy.

Treatment for Glue Ear 1. Many children recover naturally from glue ear once the Eustachian tube opens. Doctors usually adopt a wait-and-see approach to begin with. Your child will normally be observed for about three months to see if they need further treatment. If the eardrum has burst, it should heal over time approximately 3-6 weeks. 2. Self medication can be performed by means of an OTC pediatric oral decongestant to thin the fluid in the ear and help it drain away. The main purpose of a decongestant is to dry the nasal passages so the Eustachian tube opens and the fluid drains into the throat. If that does not work you might want to try a small dose of an antihistamine such as Benadryl. Have your pharmacist recommend a child's dosage. If that treatment still doesn't work, see your family doctor or physician. They might prescribe stronger antihistamines or nasal steroids in the form of drops or sprays - both of which will help reduce the swelling of the Eustachian tube.

3. The second treatment is if there is a suspected infection. If the eardrum has burst, this is usually the case. Antibiotics are sometimes prescribed, often initially by injection, then a regimen orally three times a day for at least 7 days. In the past, antibiotics such as penicillin, erythrosine, or erythromycin were prescribed. However, in the last few decades, many in the general population have become immune to the effects of these antibiotics, and stronger ones are often prescribed. (The cause of immunity is often blamed on antibiotics fed to the food supply (chickens and beef) before they are brought to market). Surgical Treatments for Glue Ear

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Grommets-myringotomy If your child has had glue ear over a few months and the eardrum has not burst and antibiotics have not worked, the other option is to have a small ventilation drain known as a grommet inserted into the ear drum. The grommet is made of either stainless steel or plastic. This procedure involves making a small hole in the eardrum and inserting the grommet through the hole to keep it open. Initially fluid is sucked out of the middle ear through this hole, then over a few months, the grommet lets air into the middle ear space and lets fluid in the middle ear drain away. There are only simple precautions to stop water getting into ear like swimming on the surface of the water only and not dive and you need to use earplugs or cotton wool with Vaseline to stop soap water getting into the ears when showering or washing hair.

Plastic grommet to drain middle ear fluids

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Adenoidectomy

It is a surgical treatment for glue ear which aimed to remove the adenoids. The adenoids are located above the tonsils, at the back of the throat and are thought to assist the body in its defense against incoming bacteria and viruses by helping the body to form antibodies. With ear infections, the adenoids often swell, usually due to an infection in the immediate area, in this case, the middle ear.

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Tubo-Tympanic Otitis Media The tubo-tympanic form usually involves a perforation of the central part of the eardrum. This can be caused by infection, injury or surgery. Symptoms of tympanic otitis media (triad)

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Hearing loss Discharge (which may come and go, and will become noticeable particularly if you get a cold or the ear gets wet) Tinnitus.

Treatment of tympanic otitis media If the opening is not too large, it may close and heal on its own. Failing that, an ENT specialist may close it with surgery or by covering it with a special material to keep the opening closed while it heals. You can usually help the symptoms by taking simple steps like wearing an ear plug or keeping the ear dry when you are having a bath or swimming. However, you may need an operation to repair the hole in the eardrum (tympanoplasty or myringoplasty).

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Attico-antral The attico-antral form of CSOM might also involve a hole in the eardrum usually in the upper part. This form of CSOM can be more of a problem than the tubo-tympanic form because the eardrum sheds dead skin which can build up and enter the middle ear. There are two major complications of the attico-antral variant of CSOM - Cholesteatomas and Mastoid infections (Mastoiditis).

 Burst Eardrum (Perforation of eardrum, Rupture of the tympanic membrane) In the final stages of a middle ear infection, if the pressure becomes too much, the eardrum may burst. This is actually a positive event if controlled properly. The burst eardrum will immediately relieve the pressure in the middle ear and the accompanying earache will diminish. A smelly discharge (bacteria detritius from the middle ear) will spill out of the ear and can be sopped up with a wet rag or a tissue.

Causes of a burst eardrum

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External Causes of a Burst Eardrum - An external cause for a burst eardrum is a head trauma such as a blow to the ear or an object penetrating the ear canal and penetrating the eardrum. Usually, the larger the perforation, the greater the loss of hearing. The location of the perforation in the eardrum also affects the degree of hearing loss. If severe trauma (skull fracture) disrupts the bones in the middle ear which transmit sound or causes injury to the inner ear structures, the loss of hearing maybe quite severe. With a traumatic or explosive event, the loss of hearing can be great and tinnitus may be severe. Side effects of a perforated eardrum will definitely be excruciating pain. You will probably also suffer from vertigo and tinnitus Internal Causes of a Burst Eardrum- Perforated eardrums from internal causes are usually from middle ear infections or otitis Media. Detritus from the infection in the inner ear causes pressure to build in the middle ear cavity and if not relieved, the eardrum will burst outward.

Symptoms of a burst eardrum from internal causes • • • • • • •

Sharp pain as the eardrum bursts, then initial pain relief. Pus discharge from the ear, and usually very smelly Bleeding from the ear Hearing loss Tinnitus Vertigo Throbbing pain as the middle and inner ear is subject to direct contact with the air

Treatments for a Burst Eardrum

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If you have had a middle ear infection that pushed out the eardrum, then the throbbing pain has been greatly diminished. Wipe off the smelly pus with a damp cloth, and sit quietly with a warm compress on that side of the head. Antibiotics are usually prescribed, sometimes initially by injection, then a regimen orally three times a day for at least 7 days. If the perforation is very small and it does not heal after 2-3 weeks, an ENT may decide not to operate and allow nature to take its course and let the eardrum heal naturally. For a larger tear, an outpatient visit to the ENT will allow a small patch (taken from under the skin behind the ear perhaps) to be attached (not completely covering the hole) over the hole to help it shrink and encourage new skin growth. Another technique an ENT may use to encourage healing is to add a chemical to the edges of the hole to stimulate growth and then place a thin paper patch on the eardrum to act as a base for skin growth over the hole. There are a variety of surgical techniques, but all basically place tissue across the perforation allowing healing. The name of this procedure is

called tympanoplasty or myringoplasty. Surgery is typically quite successful in closing the perforation permanently, and improving hearing.

Allowable sound exposure times

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Maximum Hours of Exposure Per 8-Hours Workday 24 hrs. 16 hrs. 12 hrs., 40 mins. 10 hrs., 04 mins. 8 hrs. 6 hrs., 21 mins. 5 hrs., 03 mins. 4 hrs. 3 hrs., 10 mins. 2 hrs., 31 mins. 2 hrs. 1 hr., 34 mins. 1 hr., 16 mins. 1 hr. 48 mins. 38 mins. 30 mins. 24 mins. 19 mins. 15 mins. 12 mins. 9 mins., 6 secs. 7 mins., 30 secs 3 mins., 45 secs 1 min., 52 secs 56 secs 28.07 secs 14.03 secs 7.01 secs 3.31 secs 1.45 secs .52 secs .26 secs .13 secs .06 secs

 Mastoid Infection (Mastoiditis) The mastoid is part of the skull and is made up of spongy bone just behind the ear. Mastoiditis is an infection of the bony air cells in the mastoid bone. In fact the middle ear and the inner ear are embedded in the mastoid bone. Indications of a mastoid infection are reddening and swelling behind the ear. The cause is usually from an untreated middle ear infection, so otitis media symptoms are often present. An untreated middle ear infection can slowly spread into the mastoid cells. When infection becomes trapped in the mastoid it is known as mastoiditis.

Another example showing a child's Note the mastoid bone right ear being pushed forward by swelling behind the ear the mastoid infection Symptoms of mild mastoiditis • • •

Reddening behind the ear Swelling Sensitive to touch.

Symptoms of acute mastoiditis • • • • • • •

Pronounce bulbous swelling that can push the ear forward (acute) Large swelling behind the ear High fever Ear pain Sensitive to touch Hearing loss Paralyzed facial nerves (serious cases)

Treatment for Mastoiditis Antibiotics are the normal treatment for the mild form of mastoiditis. There are a number of antibiotics available to treat. Because there are few blood vessels permeating the mastoid area, a normal 10 day protocol of antibiotics may be extended to 14 days to make sure the medicine penetrates the bony mass. While in acute form mastoidectemy is inevitably needed.

Diagnostic Procedures for Mastoiditis A number of procedures will usually be performed in a hospital setting to ascertain the extent of the disease's progress and to rule out any complications. A CTscan and X-rays will be used to assess the extent of the infection. To assist with diagnostic procedures an antibiotic therapy through IV is needed, and if the eardrum has not burst, a small incision will be made in the eardrum (myringotomy) to allow drainage of the infection. Mastoid Surgery -Mastoidectomy A mastoidectomy is done under general surgery. It involves drilling away the infected bone. This aims to remove all the infected bone. An incision is made behind the ear and the flap is lifted forward. A circle is cut out of the bone covering the mastoid and showing the infected area. The spongy mass that is infected is then cut away and removed. The remaining cavity is cleaned, coated with antibiotics and if possible the bone cover is place back to the rest of the skull, and the flap of skin stitched back together. An outer pressure dressing is then worn for 1-2 days after surgery. If too much mastoid material has been removed, and it is not possible to reattach the bone covering, it is left off and the skin flap is stitched back to the surrounding tissue. After healing, there will be depression behind the ear.

The stay in the hospital is usually 1-3 days. After discharged from the hospital, a full regimen of antibiotics will be given (10-14 day regimen). The stitches will be removed after about 2 weeks. Full recovery will take 3-4 weeks with possibly bouts of dizziness and headaches during this time. Over time the headaches and dizziness should diminish.

 Cholesteatoma A cholesteatoma occurs if skin from the inner side of the tympanic membrane sloughs off and mixes with ear wax that penetrates the open hole in the eardrum to the middle ear chamber and fails to drain through the Eustachian tube. Over time the accumulation of dead skin and wax causes a cyst-like mass to grow -cholesteatoma. If left untreated and the mass becomes larger, the mass can put pressure to nearby parts of the ear causing serious damage such as the eardrum and ossicles. In serious cases, cholesteatomas have been known to penetrate into the mastoid area causing infection or into the cranial chamber causing meningitis-infection of the covering of the brain or the meninges.

Symptoms The attico-antral form of the condition initially causes a smelly discharge to leak from the ear. You may also have a hearing loss and sometimes tinnitus. You can get vertigo dizziness - if the semicircular canals, which form part of the balance system, are also affected. Signs of cholesteatoma • • • • •

Extreme pain, especially in the side of the head where the problem is Continual vertigo and nausea Loss of hearing A gradual weakening of the facial muscles causing a droopy look on one side as if recovering from a stroke Headaches similar to migraines

Treatment for Cholesteatoma It is important to remove the cholesteatoma and all traces of infection. For this, it is usually necessary to have a surgical procedure known as mastoidectomy. Once the middle ear chamber is opened, the mass is removed and the surgeon will check to make sure the ossicles are not damaged and that the cholesteatoma has not penetrated to other areas of the cranium.

 Damaged Ossicles (Ossicular Chain Disruption)

Causes of Damaged Ossicles • •

Trauma to the ear drum from external sources. Continuous infections can slowly dissolve one or all three of the bones that make up the ossicles.

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Genetics: Babies are sometimes born with malformed ossicles. They can be repaired or replaced by having an operation called an ossiculoplasty.

Surgical Procedures (Ossiculoplasty) As with mastoid surgery, an incision is made behind the ear and a flap of skin pulled back to access the inner ear chamber. The damaged ossicles is removed and matched against various sized artificial bones to get a close match. Titanium is often used to replace one or more of the bones and is custom fitted for each patient’s unique bone lengths. Titanium is used as the body will not reject the metal and after time will actually grow a slime covering over the metal. The ossicles are very small and this makes the surgery very delicate. Patients are put under local or general anesthesia in a hospital and the implant procedure usually lasts about two hours. Because of the small size of the bones and the small workspace of the middle ear (about a 1" chamber), surgery is performed using a special microscope. For more serious middle and inner ear operations that are performed under general surgery, robotic machines are used.

 Otosclerosis Otosclerosis is a spongy bone-like tissue that grows at the place where the stapes meets the oval window of the cochlea. As this growth grows, it slowly prevents the ossicles from moving well. Otosclerosis is the most frequent cause of middle ear hearing loss and affects about 10% of the United States population. It is most commonly seen in more women than men often during pregnancy, implying a hormonal cause. Caucasians are more likely to have this disorder than any other race. Only 1% of African Americans have otosclerosis. It is also rare among Orientals and Native Americans.

Image of otosclerosis occurring between the stapes and the oval window of the cochlea Causes of Otosclerosis The causes of otosclerosis are not exactly known. However, the most generally accepted theory is that it has a genetic basis, combined with hormonal production abnormalities. The gene that cause the otosclerosis appears to be a dominant, rather than a recessive gene, but it has a characteristic called

“reduced penetrance” meaning it does not always dominate over a normal gene. At first, hearing loss occurs in the low frequencies. High frequencies are affected next, followed by the loss of hearing in the middle frequencies. Otosclerosis usually begins in one ear, but the other ear often develops it as well. If left untreated, otosclerosis will cause the hearing to steadily get worse and can lead to profound deafness. It is rare for otosclerosis to occur after the age of fifty. Categories of Otosclerosis

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Subclinical Otosclerosis- occurs when the tissue does not interfere with the ossicles. A person may have this form for many years and not know it. Clinical Otosclerosis- This type can be present in the teen years, but not detected until the young adult years. Histologic Otosclerosis- occurs when the tissue is present, but it does not grow larger. This rare condition may or may not cause a hearing loss. Very occasionally, otosclerosis can also affect the inner ear. The condition can affect either one, or more commonly, both ears.

Symptoms of Otosclerosis • • • •

Tinnitus Hearing loss, often at lower frequencies You may also find that your hearing is better in noisy surroundings. People with otosclerosis tend to speak quietly.

Treatments for Otosclerosis In the early stages of otosclerosis, or when the condition is mild, you might not need any treatment. Hearing aids are very useful initially. However, as the tissue builds up on the stapes you will gradually lose your hearing. Sodium fluoride tablets have been shown to help prevent the progression of otosclerosis, but only if the condition has also affected the inner ear. Surgical procedures for Otosclerosis

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Stapedectomy- this operation aims to improve hearing by replacing the stapes one of the ossicles, with a piston. The piston helps to restore the movement of the ossicles, so transmitting sound into the inner ear.

Most of the stapes bone is removed, leaving just the portion called the footplate, which sits in contact with the oval window. The oval window is the link between the middle and inner ear. A small hole is then drilled in the footplate and the piston is inserted so that it sits in contact with the oval window. At its other end, the piston is attached to the incus, the middle of the three ossicles. About 85% of people find the operation a success and report a good improvement in hearing. However, there is a very small risk of fluid loss in the years following surgery -for example, if you have a sudden blow to the head or sudden pressure change that causes the piston to penetrate the membrane of the oval window.

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Fenestration- the idea of the operation is that since the oval window is obliterated by bony growth, a new window (fenestra) needs to be made, and usually this window is to be drilled into the lateral semicircular canal level of the promontory.

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Stapedolysis (stapes mobilization) - The principle of this surgery is so simple, if the stapes is stuck, free it. The procedure involves raising the tympanic membrane, exposing the contents of the middle ear, attaching the hook like instrument to crus of the stapes, and by jerking it, freeing the footplate from the otosclerosis growth.

COMMON DISEASE AND DISORDER OF THE INNER EAR

It is estimated that up to 25% of any population in the industrialized world will experience dizziness, with or without vertigo, at some point in their lives. Older people experience it more than the younger population. It is important to understand that all vertigo comes with dizziness, but not all dizziness comes with vertigo.

 Dizziness The main symptoms of dizziness include a feeling of light headedness. There are numerous reasons why a person may be experiencing dizziness. It may be related to anxiety or panic disorders, or mood disorders. Dizziness in the form of light-headedness may result from a cardiovascular problem such as an irregular heart beat (arrhythmia) or if your blood pressure drops when you change positions (postural hypotension). There are some medications that may cause light-headedness or imbalance such as some blood pressure medications (antihypertensives), medications to control convulsions or spasms (anticonvulsants), calming medications (sedatives) or medications that help with sleep (hypnotics). Problems with chemical changes within your body (metabolic problems) may also cause dizziness, such as if your blood sugar drops too low (hypoglycemia) or hormonal imbalances. Symptoms of Dizziness • Light headedness • Motion sickness or nausea • Faintness or weakness

 Tinnitus Another symptom that is sometimes associated with true vertigo is tinnitus. Tinnitus is noise in the ear that may be heard on and off, continuously or in a pulsation

form. This noise may be buzzing, ringing, roaring, whistling or hissing. It often goes with many ear disorders, including Meniere’s disease, infections such as an inflammation of the middle ear -otitis media, or inflammation of the internal ear –labrynthitis, eustachian tube obstruction or noise-induced hearing loss. Two general classes of Tinnitus

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Vibratory- appears when the underlying etiology originates from outside the patients like loud noise and head trauma. Nonvibratory – appears when the cause is due to disease, drugs or some other internal process The Semi-Circular Canals as Balancers

The body senses its different positions and controls its balance through organs of equilibrium (balance) that make you feel stable, or normal. These organs of balance are located in the inner ear and are called the semicircular canals. These canals look like loops of tubes. Their connections on one side are to the cochlea where they receive sounds, and to the aural nerves going to the brain. The semicircular ducts are arranged roughly at right angles with each other so that they represent all three planes in three-dimensional space. The horizontal duct lies in a plane pitched up approximately 30 degrees from the horizontal plane of the eartherect head. The front canals are located in vertical planes that project forward and outward by approximately 45 degrees. The rear canals are located in vertical planes that project backward and outward by approximately 45 degrees.

If you could take the upper portion of each inner ear on each side of the head, they would be symmetrical the front canal on one side of the head is parallel to the rear canal on the other. Messages to the brain as to the head's changes in position are generated by calcium carbonate crystals that shift on their bed of sensory hairs in the utriculus and the sacculus. The changes as to which hairs are being stimulated by the presence of

crystals are reported to the cerebellum which in turn, translates the information into knowledge of the position of the head relative to gravity.  Vertigo A major symptom of a balance disorder, it is the sensation of spinning or swaying while the body is stationary with respect to the earth or surroundings. The word “vertigo” comes from the Latin “vertere” to turn and “igo”, a condition, meaning a condition of turning about. Two classes of vertigo:

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Subjective vertigo- is when a person feels a false sensation of movement. Objective vertigo- is when the surroundings will appear to move past a person's field of vision

Symptoms of True Vertigo • • • • • •

Sense of movement An illusion of spinning and circling Worsened with head movements Nausea/vomiting Episodes come and go Rhythmic Eye Movement (Nystagmus)

Causes of Vertigo The cause of all vertigo is when the semi-circular canals are not functioning properly, ether due to infection, inflammation, trauma, hormonal imbalances, blood disorders, or scarring. However, for vertigo that lasts off and on or continuously for a few days, the following are some probable causes. • • •

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Low tolerance for vehicular motion such as cars, boats, cruise ships, and airplanes that cause motion sickness. A head cold or some infection of the ear or nasal passages that blocks or swells the eustachian tube. The subsequent inability of the middle ear to equalize air pressure in the middle ear chamber causes undue pressure on the inner ear, and subsequently the semicircular canals where balance is registered. High blood pressure High cholesterol Diabetes Anemia Calcium disorders Alcohol or drug abuse Brain tumors and Syphilis (rare cause)

Most Common Types of Vertigo

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Meniere’s Disease

Vertigo with hearing loss on one-side, noise in the ear and aural fullness. Meniere’s Disease is an inner ear disorder that brings spontaneous episodes of vertigo that can last minutes to hours. Along with the vertigo, there may be some hearing loss in the affected ear that comes and goes, as well as an increase in tinnitus and a sense of fullness in the Meniere’s affected ear. Between episodes, you may have a persistent hearing loss and tinnitus in the affected ear. The vertigo associated with Meniere’s Disease may happen suddenly, or may build in intensity over several hours and you may begin to experience nausea or vomiting. Causes of Meniere's Disease The underlying cause of Meniere's Disease is unknown. Meniere's Disease is felt to be due to an abnormality in the fluid balance of the inner ear. Symptoms of Meniere's Disease • • • •

Lasts minutes to hours Usually an accompanying hearing loss or a change in hearing Tinnitus Feeling of pressure in ears

Possible Treatments for Meniere’s Disease 

The first is to treat the symptoms of vertigo with anti-vertigo medication. Often an anti-nausea agent is necessary to combat the sick feeling that comes with vertigo. During and following a vertigo attack, the affected patient should avoid movements as they may increase the severity of the symptoms.

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The second form of treatment is prevention of further vertigo attacks. Certain medications are effective in reducing the frequency and severity of vertigo attacks. Surgery may be necessary to treat Meniere's Disease. One option is having surgery to place an antibiotic directly into the inner ear. This may reduce the attacks of vertigo.

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Lifestyle and Diet Changes There are some changes to diet and lifestyle that may help you manage Menire's Disease. These include a low-salt diet to help reduce fluid retention as well as taking a medication that encourages urination. You should also avoid sudden movements as they may aggravate these symptoms.

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Recurrent Vestibulopathy

Severe vertigo, with or without hearing loss Patients who suffer multiple episodes of severe vertigo without hearing loss likely have what is known as recurrent vestibulopathy. These attacks of vertigo come and go, and last from minutes to hours. This disorder is therefore similar to the later, but without any hearing loss or noise in the ear. There is no evidence of brain dysfunction with recurrent vestibulopathy, and it usually goes away over time. Some recurrent vestibulopathy may turn into Meniere's Disease or benign paroxysmal positional vertigo (BPPV). Causes of Recurrent Vestibulopathy The cause or causes of recurrent vestibulopathy are unknown. Symptoms of Recurrent Vestibulopathy • Lasts minutes to hours • No hearing loss or tinnitus Treatments for Recurrent Vestibulopathy Treatment for recurrent vestibulopathy is similar to Ménière's Disease. These may include an anti-vertigo medication and anti-nausea agent to combat the sick feeling that comes with vertigo. There are some changes to diet and lifestyle that may help you manage this type of vertigo. These include a low-salt diet to help reduce fluid retention as well as taking a diuretic.

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Benign Paroxysmal Positional Vertigo or BPPV

Vertigo caused by free floating particles in the inner ear organ of balance or vestibule

Debris in the posterior semicircular canal of the inner ear (BPPV) The vestibular system located in and around the ear controls our body's sense of balance. When your head moves, the vestibular system sends information to the organs inside the ear, and these organs then pass the information on to the brain. Symptoms of BPVV Benign paroxysmal positional vertigo (BPPV) results from debris particles that move freely within fluid in the canals of the inner ear. The debris is not related to getting anything in the ear canal, it just forms on its own. A change in your head position, lying down, getting up, turning over in bed, or tipping your head backwards to look up may cause the debris to shift. This shifted debris affects the balance receptor in the ear and causes vertigo. The vertigo associated with BPPV comes on suddenly and usually only lasts for seconds to minutes. There are usually no hearing symptoms. Possible Treatments for BPPV A skilled doctor can perform some maneuvers that can move the debris out of the sensitive part of the ear (posterior canal). Your doctor can also teach you how to do certain exercises at home, placing your head in various positions at different angles. This may help move the debris in your ear as well. The need for surgery is very rare, but in such cases a procedure known as “posterior canal plugging” can be done. This blocks most of the canal’s function, which can reduce the symptoms.

 Vestibular Neuronitis

Disruption of vestibular input to the brain The brain and the inner ear communicate information via nerves. The cochlear nerve carries information about noise and hearing, the vestibular nerve carries information about balance and body position. Viruses can affect either or both nerves and the symptoms will vary according to which nerve has been affected. Vestibular neuronitis is an inflammation of the vestibular nerve that causes a disruption of the message sent by the vestibular nerve to the brain. The first attack of vertigo is usually severe, and is associated with nausea and vomiting, lasting days to weeks. People with vestibular neuronitis do not have hearing loss or tinnitus.

Symptoms of Vestibular Neuronitis • Vertigo Lasts days to weeks • No hearing changes

 Viral Labyrinthitis Viral infection of the inner ear It is a sudden disruption of the messages to the brain from within the inner ear as a result of a sudden viral infection. As a result of this virus, you may experience severe vertigo that usually comes on suddenly and can last from days to weeks, depending on the length of time the body builds up anti-bodies to the virus. There are no other symptoms related to the ear. Symptoms of Viral Labyrinthitis • Vertigo Lasts days to weeks • May have hearing changes Possible Treatments for Either Cause

It is important for people suffering from such symptoms to be examined and diagnosed by an ENT specialist since other conditions, such as stroke can present with similar symptoms. There are several medications that your physician may recommend if they feel that the vertigo associated with the vestibular neuronitis or viral labyrinthitis requires treatment. These include anti-vertigo agents, antihistamines, sedatives and or anti-nausea agents. There are some other things that you can do to help alleviate the symptoms. Bed rest is recommended for the first 2 to 3 days from the initial onset of your symptoms. If your vertigo symptoms last more than a few days, staying active may be more helpful. There are also some exercises that your doctor may suggest once the vertigo has subsided. Viral diseases that cause hearing loss:  Cytomegalovirus  Mumps  Acquired Immunodeficiency Syndrome  Herpes Bacterial diseases that cause hearing loss:  Meningitis  Syphilis Hearing loss associated with systemic disease  Thyroid Disease  Diabetes Mellitus  Kidney Disease  Multiple Sclerosis  Connective Tissue Disease  Meniere’s Disease PEDIATRIC DEAFNESS Normal hearing requires that all parts of the auditory pathway are working correctly. This pathway includes the external ear, middle ear, inner ear, auditory nerve, and the connection between the auditory nerve and the brain. The exact location and nature of the problem in the auditory pathway determines the type and severity of a person's hearing loss. Some causes of hearing loss occur before a baby is born. These include genetic disorders such as Warrensburg syndrome or Crouzon syndrome and infections such as congenital rubella or congenital syphilis. Genetic Factors About half of all cases of hearing loss among children are thought to result from genetic factors. Sometimes these children have a syndrome of which hearing loss is only one feature. However, in most children with hearing loss that is due to a genetic cause, the

hearing loss is not part of a syndrome. A variant of the connexin 26 gene is responsible for much of the hearing loss in this latter group of children. Postpartum Factors Problems during or soon after birth can also be risk factors for developing hearing loss. These include hypoxia, bleeding in the brain, and hyperbilirubinemia. Children who are born early or at low birth weight are more likely to have problems that may lead to hearing loss. However, children who are normal birth weight can have hearing loss. Other Factors Hearing loss can also occur later in a child's or adult's life. Causes during this time include infection such as meningitis, chronic middle ear infections, or measles, injuries such as head injury, or certain drugs such as the antibiotic gentamycin. High noise levels such as from firecrackers or loud rock concerts can also damage a person's hearing. About 30 million workers are exposed to dangerous noise levels on their jobs. Another nine million are at risk of hearing loss as a result of working with certain metals or solvents. Some causes of hearing loss can be prevented. For example, vaccines can prevent certain infections, such as H-flu meningitis or measles, which can cause hearing loss.

The Technology of Hearing Aids

• Body worn aids This was the first type of hearing aid invented by Harvey Fletcher while working at Bell Laboratories. These aids consist of a case containing the components of amplification and an ear mold connected to the case by a cord. The case is about the size of a pack of playing cards and is worn in the pocket or on a belt. Because of their large size, body worn aids are capable of large amounts of amplification and were once used for profound hearing losses.

• Behind the ear aids (BTE) BTE aids have a small plastic case that fits behind the ear and provides sound to the ear via air conduction of sound through a small length of tubing, or electrically with a wire and miniature speaker placed in the ear canal. The delivery of sound to the ear is usually through an earmold that is custom made, or other pliable fixture that contours to the individual’s ear. BTEs can be used for mild to profound hearing losses and are especially useful for children because of their durability and ability to connect to assistive listening devices such as classroom FM systems.

• In the ear aids (ITE) These devices fit in the outer ear bowl or pinna they are sometimes visible when standing face to face with someone. ITE hearing aids are custom made to fit each individual's ear. They can be used in mild to some severe hearing losses. Feedback, a squealing/whistling caused by sound leaking out of the aid and being amplified again, may be a problem for severe hearing losses. Some modern circuits are able to provide feedback regulation or cancellation to assist with this. Traditionally, ITEs have not been recommended for young children because their fit could not be as easily modified as the earmold for a BTE, and thus the aid had to be replaced frequently as the child grew.

• Receiver In the ear aids (RITE) At a first glance, these devices are similar to the BTE aid. There is however one crucial difference, the receiver of the hearing aid is placed inside the ear canal of the user and thin electrical wires replaces the acoustic tube of the BTE aid. There are some advantages with this approach. First, the sound of the hearing aid is arguably smoother than that of a traditional BTE hearing aid. With a traditional BTE hearing aid, the amplified signal is emitted by the receiver which is located within the body of the hearing aid behind the ear. The amplified signal is then directed to the ear canal through an acoustic tube, which creates a peaky frequency response. With a RITE hearing aid, the receiver is right in the ear canal and the amplified output of the hearing aid does not need to be pushed through an acoustic tube to get there, and is therefore free of this distortion. Secondly, RITE hearing aids can typically be made with a very small part behind-the-ear and the wire connecting the hearing aid and the receiver is extremely inconspicuous. For the majority of people this is one of the most cosmetically acceptable hearing device types.

• In the canal (ITC) and completely in the canal aids (CIC) ITC aids are smaller, filling only the bottom half of the external ear. You usually cannot see very much of this hearing aid when you are face to face with someone. MIC and CIC aids are often not visible unless you look directly into the patient’s ear. These aids are intended for mild to moderately-severe losses. CICs are usually not recommended for people with good low frequency hearing, as the occlusion effect is much more perceivable.

• Open-fit devices "Open-fit" or "Over-the-Ear" OTE hearing aids are small behind-the-ear type devices. This type is characterized by a small plastic case behind the ear, and a very fine clear tube running into the ear canal. Inside the ear canal, a small soft silicone dome or a molded, highly vented acrylic tip holds the tube in place. This design is intended to reduce the occlusion effect. Conversely, because of the increased possibility of feedback, they are limited to moderate high frequency losses.

• Bone Anchored Hearing Aids (BAHA) The BAHA is an auditory prosthetic which can be surgically implanted. The BAHA uses the skull as a pathway for sound to travel to the inner ear. For people with conductive losses, the BAHA, bypasses the external auditory canal and middle ear, stimulating the functioning cochlea. For people with unilateral hearing loss, the BAHA uses the skull to conduct the sound from the deaf side to the side with the functioning cochlea. The implant vibrates the skull and inner ear, which stimulate the nerve fibers of the inner ear, allowing hearing.

• Eyeglass aids Recently, a new type of eyeglass aid was introduced. These “hearing glasses” feature directional sensitivity: four microphones on each side of the frame effectively work as two directional microphones, which are able to discern between sound coming from the front and sound coming from the sides or back of the user. This allows for amplification of the sound coming from the front, the direction in which the user is looking, and active noise control for sounds coming from the sides or back. Only very recently has the technology required become small enough, in size, to be put in the frame of the glasses.

Hearing aids are built from analog or digital circuits. Each technology processes sound differently. Until recently, all hearing aids were analog. Digital hearing aids are the newest kind of hearing aid and are superior to analog. All hearing aids, whether analog or digital, are designed to increase the loudness of sounds reaching the ear drum so that the hearing-impaired person can better understand speech. Components of Hearing Aids

1. A microphone to gather acoustic energy (sound waves in the air) and convert it to electrical energy. 2. An amplifier to increase the strength of the electrical energy. 3. A receiver, which is like a miniature speaker that converts the electrical energy back into acoustic energy (sound waves).

Difference between digital hearing aids and analog hearing aids in terms of functioning Analog Hearing Aids

Analog hearing aids use a continuously varying electrical signal to produce sound, just like a microphone and loudspeaker. Analog hearing aids have a microphone that picks up sound and converts the sound into small electrical signals. These signals vary according to the pattern of the sound. The signals are then amplified (made louder) by transistors and fed to the ear phone on the hearing aid which is next to your ear drum so you can hear them. Most of the better analog hearing aids compress the sound using “automatic gain control” (AGC). This amplifies quiet sounds until they are loud enough to be heard, but gives less amplification to sounds that are already loud, so you're protected against uncomfortably loud sound levels. Analog hearing aids don’t have all the features that come with advanced digital aids, but they are less expensive.

Digital Hearing Aids

Digital aids take the signal from the microphone and convert it into "bits" of data numbers that can be manipulated by a tiny computer chip in the hearing aid. This makes it possible to tailor and process sounds very precisely in ways that are impossible with analog aids. The digital chip takes the bits representing the sound and analyzes and manipulates them using what is called DSP or Digital Signal Processing. Software algorithms (a set of instructions), are used to perform the precise complex DSP actions, and are then converted back into electricity, which is finally changed back into sound that goes into the ear. This process happens very rapidly with several million calculations occurring in the hearing aid each second. The digital sound representations can be manipulated in almost any way imaginable, and this is what gives the digital hearing aid its big advantage. When someone talks, you usually want to hear what they are saying, rather than whatever noise is going on in the background. People who use traditional analog hearing aids often complain that they find it difficult or impossible to follow conversations in noisy places. Many digital aids are designed to reduce steady kinds of background noise, such as crowds in a restaurant or the rumble of traffic or the whirr of a fan. This makes listening more comfortable. But it does not necessarily help you to pick out a single voice from everything else that's going on, especially when several people are talking. Some digital hearing aids also have circuitry to protect whatever hearing is left. If a loud sound is detected above the 90-100 Db range which can cause damage, dampening circuitry cut out the sound. To effectively use any sensory aid, clients must know and understand the following: 1. Component parts and their specific function. 2. Benefits and limitation of available sensory aids. 3. How to clean and maintain the aid for daily use. 4. How to troubleshoot the operation and performance of selected aids. 5. How to adjust the aid for everyday use. 6. How to mange minor problem. 7. Who to contact in the event of a problem with the aid. 8. Cost of replacement aids and batteries on how to acquire them. 9. How to use aids in combination to enhance the performance over a single aid.

10. Insurance and manufacturer warranty conditions. COCHLEAR IMPLANTS Advances in computer technology as well as in ear surgery itself have given us the opportunity to offer the world of sound, music, and speech to those who would otherwise have spent their lives in a soundless cocoon. Those who are born deaf prelingual deafness, as well as children and adults who lost their hearing from either disease or trauma post lingual deafness, can experience the gift of hearing thanks to cochlear implants. Development of the devices came about through the surgical experiments of a group of French medical scientists as well as the pioneering work of William House of Los Angeles, Dr. Robert Schindler of San Francisco and a cochlear implant team from Melbourne Australia. Miniaturization and advances in computer technology over the last 30 years set the stage for the further development of more sophisticated and effective cochlear implant devices. Today, over 30,000 individuals have been implanted worldwide, over 3,000 cochlear implants were performed in 1999 alone.

Sound is picked up through a tiny microphone housed in a headpiece that is worn at the ear. The sound is sent along a cable to a processor, a mini-computer that converts the sound into digital signals. The processor is worn on the belt or, in some models at ear level. Once processed, the digital signals go back up to a transmitter (in some models, the transmitter and the microphone are in the same piece in other models, the microphone is in a behind-the-ear piece that looks like a conventional hearing aid). The transmitter, which is held by a magnet on the side of the head behind the ear, sends the coded signals via radio waves across the skin to the implant. The implant delivers the

signals to electrodes that have been inserted into the cochlea. The electrodes stimulate the auditory nerve, sending impulses to the brain where they are interpreted as sound.

Initial experiments with deaf participants indicated that if an electrode was placed on the bony wall of the inner ear and an electric current was passed through the electrode, the deaf individual could perceive the sensation of sound. From this very basic observation the concept of placing an active electrode into the inner ear by way of the round window -the only non-bony entry into the cochlea of the inner ear was born. Initial implants were thus placed against the outer wall of the inner ear. Soon, they were introduced into the cochlear chamber itself through the round window. Not only was this introduction more effective in stimulating the residual nerve endings of the inner ear, but it also allowed the surgeon to better anchor the implant into the inner ear without risk of loosing contact with the nerve endings. Individuals with deafness usually have lost most of their “hair cell” nerve endings which normally conduct sound from the ear to the brain. Significant residual nerve endings are needed to be present in the deaf to allow for their direct stimulation by the neighboring electrodes. The cochlear implant is thought to function by directly stimulating the surviving nerve population in the cochlea and spiral ganglion.

The earliest cochlear implants consisted of a single active electrode, introduced into the inner ear, through the cochlear wall next to the round window. Today, most investigators in the cochlear implant field agree that stimulating the residual nerve cell population with multiple electrodes at different sites within the cochlea, combined with

sophisticated computer assisted processing strategies allows for better recognition and understanding of speech. Both the Nucleus 24 Contour and the Clarion High Focus devices have further refined this concept with the closer placement of the electrode array to the residual spiral ganglion cells of the auditory nerve.

The active electrodes in these newest devices allow them to hug the bony inner wall of the cochlea instead of loosely fitting into the cochlear chamber. This concept may allow for lower electrical stimulation levels of individual electrodes which would prevent “cross chatter” between electrodes (jumping of electrical fields from one electrode to another) and conserve battery life as well. Long lasting batteries requiring little electric current will allow for a completely implantable cochlear device in the future. For the present, the implantable portion includes the electrode array and wire from the electrodes to an implanted portion of the device which is behind the ear. The remaining hardware of the device includes the microphone, receiver, speech processor and magnetic link between the outer scalp and the implanted portion of the device. The external portion of the unit receives and processes sounds which are then fed into a specific electrode pair. These, in turn, stimulate the auditory nerve and finally the auditory center of the brain.

OLFACTION Anatomy and Physiology NOSE The nose is the organ involved in smell and breathing. It is located in the middle of the face. The internal part of the nose lies above the roof of the mouth. It processes the air that you breathe before it enters your lungs. Most of this activity takes place in and on the turbinates, located on the sides of the nasal passages. In an adult, 18,000 to 20,000 liters of air pass through the nose each day.

The nose is consists of:

    

External Nose- triangular-shaped projection in the center of the face. Nostrils - The two openings into the nasal passages. Nasal passages - passages that are lined with mucous membranes and tiny hairs (cilia) that help to filter the air and move nasal and sinus mucous to the back of the throat. Nasal passages are separated by the nasal septum. Septum - made up of cartilage and bone and covered by mucous membranes. The cartilage also gives support to the lower part of the nose and divides the nasal passages into right and left sides. Sinuses - four-paired, air-filled cavities.

Sinuses The sinuses are cavities, or air-filled pockets inside the face, near the nasal passages. As in the nasal passages, the sinuses are lined with mucous membranes. There are four sinuses:

 

Ethmoid sinus - located around the area of the bridge of the nose. This sinus is present at birth, and continues to grow until puberty. Maxillary sinus - located around the area of the cheeks. This sinus is also present at birth, and continues to grow until puberty.

 

Frontal sinus - located in the area of the forehead. This sinus does not develop until around 7 years of age. Sphenoid sinus - located deep in the face, behind the nose. This sinus does not fully develop until adolescence.

ASSESSMENT of the NOSE and SINUSES The nurse uses inspection and palpation to examine the nose and sinuses. The structures assessed include the external nose, vestibule, nasal mucosa, septum, turbinates, nasal canals, and sinuses. Function of the first cranial nerve (olfactory) is usually not tested unless a deficit in the sense of smell is reported or suspected. NOSE External Nose The external nose is inspected and palpated for deviations from normal alignment, symmetry, color, discharge, nasal flaring, lesions, and tenderness. Normal

findings are listed. The skin color over the nose is the same as that of the facial skin. Alignment is straight and symmetric without deviation from midline. Discharge from the nares should be absent and the nares should not flare (spread) with respirations. The client is able to breath quietly through the nose rather than mouthbreathe. Masses, lesions, and tenderness are absent. The nurse checks the nasal canals for patency by asking the client to occlude one nares with a finger and to breathe through the open nares while closing the mouth. This is repeated for the opposite nares. The client should be able to breathe without difficulty through both nares. The nurse asks the client to tip the head back and inspects the outer nares for crusting, bleeding, or dryness, which should be absent. Internal Nose The nurse next inspects the vestibules with use of a penlight while the client’s head is tipped back. Normal findings include the presence of coarse hairs, a clear passage without discharge, and a midline septum. Further examination of the internal nose requires use of a nasal speculum; this is not done unless it is indicated. If detailed examination of the internal nose is done, the nurse either attaches a nasal speculum tip to the otoscope head or uses a metal nasal speculum and penlight for illumination. The client tips the head back, and the nurse gently inserts the speculum into one nares with care being taken not to scrape the mucosa. One nares is inspected at a time. Hold the speculum correctly and inserts the blade gently about ½ inch into the nostril. Gain additional control of the speculum by resting the index finger of the dominant hand on the side of the client’s nose. Steady the client’s head with the nondominant hand. Open the blades gently and vertically, avoiding pressure on the septum and turbinates. Slowly move the head to inspect all areas of the nasal chamber. Observe the condition of the mucous membrane (e.g., pallor, redness, swelling). Normally, the mucosa is moist and dark pink without sign of inflammation, pallor, or blue color. Presence of discharge is abnormal. The septum is midline without deviation, masses, perforation, or exudates. The turbinates (only the inferior and part of the middle turbinates are visible, the superior is not) have the same color as the mucosa and should be free of exudates, swelling, or inflammation. Look for polyps and other masses. Observe plugs of mucus for color, consistency, amount, and odor. Inspection may be hampered by nasal congestion. It may be necessary to shrink the nasal mucosa with a topical vasoconstrictor (e.g., ephedrine, cocaine, phenylephrine hydrochloride) for adequate inspection. When these agents are instilled into the nose, the client should be instructed to say “e” and hold the sound. This technique raises the posterior tongue, occludes the upper airway, and prevents the fluid from running into the pharynx. Nasopharynx The nasopharynx is best examined with a mirror with the tongue depressed with a tongue blade or gauze. Prevent the mirror’s fogging by warming it before putting it into a mouth. Hold the mirror to one side of the uvula and focus light on it. A small part of the nasopharynx can be observed with a nasal speculum. Specialists may use a nasopharyngoscope to examine the nasopharynx.

Paranasal Sinuses Assess the paranasal sinuses by (1) inspecting and palpating the soft overlying tissues, (2) observing any nasal secretions (it is possible to determine which sinus is infected according to where purulent discharge appears), and (3) transillumination of the maxillary and frontal sinuses. The nurse palpates and percusses the frontal and maxillary sinuses to assess for swelling and tenderness, which should be absent. The frontal sinuses are palpated simultaneously by placing the thumbs above the eyes, just under the bony ridge of the orbits, and applying gentle pressure. The maxillary sinuses are palpated by use of either the index and third fingers or thumbs to gently press on each side of the nose just under the zygomatic bones. Direct percussion is used over the eyebrows for the frontal sinuses and on either side of the nose below the eyes in line with the pupils for the maxillary sinuses.

TRANSILLUMINATION Transillumination is a technique to further assess the sinuses if tenderness is present. Either a penlight or the otoscope handle fitted with a transilluminator head is used. The room is darkened. The light is placed against the orbital bones immediately below the eyebrows and directed upward. The nurse shields the light source with one hand. Normally, a reddish glow appears above the frontal sinus area. Lack of illumination may indicate sinus congestion and pus accumulation. The maxillary sinuses are assessed by placing the light beneath the center of the eyes and the zygomatic bones and directing it down and in toward the roof of the mouth. The nurse asks the client to open the mouth. A glow should appear on the hard palate on the side being illuminated. For more completely assessing sinus conditions, sinus radiographs may be used. Air, normally present in the sinuses, appears as dark areas on a developed film. Smell The senses of taste and smell are closely related. Many conditions affect taste and smell, such as viral infections, normal aging, head injuries, and local obstruction. Some medications can affect smell and taste, such as metronidazole (Flagyl), local anesthetics, clofibrate (Atromid-S), some antibiotics, some antineoplastics, allopurinol, phenylbutazone, levodopa, codeine, morphine, lithium, and carbamazepine (Tegretol). Smell impairment may be (1) hyposmia (decrease in smell sensitivity) or (2) anosmia (bilateral and complete absence of smell sensitivity). Smell assessment is done by having the client identify various odors. Various substances are placed in individual test tubes (covered to eliminate visual cues). Testing each nostril separately, have the client sniff the tubes (first with eyes closed and then with eyes open). Document whether the client (1) can perceive each odor and (2) can identify each odor accurately. Smell is perceived mainly via the olfactory nerves, although some are perceived via the trigeminal nerves. Trigeminal irritants are perceived even by clients experiencing

anosmia. (Therefore, a client who claims not to smell trigeminal irritants has a hysterical loss of smell rather than hyposmia or anosmia.) DIAGNOSTIC PROCEDURES for the NOSE and SINUSES A. Flexible Rhinolaryngoscopy Flexible rhinolaryngoscopy is currently one of the most commonly used techniques for visualizing the nasal cavity, the sinuses, the pharynx, and the larynx. The technique utilizes a small-caliber flexible endoscope and can be performed in an office setting. Before the procedure, the patient's nasal cavity is decongested and anesthetized for maximum visualization and minimal discomfort. In the procedure, the examiner threads the end of the scope into the nasal aperture along the floor of the nasal cavity. As the scope is advanced, the examiner can visualize the nasal cavity proper for any evidence of lesions or masses. Once the scope approaches the nasopharynx, it is directed inferiorly and advanced slowly, allowing direct visualization of the entire pharynx and larynx. B. Functional Endoscopic Sinus Surgery (FESS) Before undergoing FESS, patients have lab tests, CT scans and other screenings to confirm the exact nature of the problem. During FESS, our otolargyngolgists (ear, nose and throat doctors) introduce an endoscope into the interior of the patient’s nose and sinuses. The slender, fiberoptic device has a tiny light at its end, enabling the physician to view the problem area. Once the instrument is positioned, tiny scalpels and other surgical tools are passed through the nostrils alongside the endoscope to remove polyps and other obstructions. Since there are no external incisions, the patient rarely experiences any bruising or swelling. C. Image-guided Endoscopic Techniques In select cases, UC Irvine Medical Center otolarngologists use image-guided endoscopic techniques. By combining the power of computerized tomography with endoscopy, they’re able to determine the anatomic location of their instruments within the sinuses and perform three-dimensional reconstructions of the surgical site. D. Sinus X-ray A sinus x-ray is a type of x-ray used to obtain images of the sinuses. The sinuses are air-filled cavities lined with mucous membranes located within the bones of the skull. During a sinus x-ray, x-rays pass through the sinuses and form an image on a special type of film. The sinuses are usually filled with air, which appears black on x-ray film. An opaque (whitened) area on an otherwise normal film may indicate the presence of sinusitis (inflammation of the mucous membranes of the sinuses), hemorrhage, tumor, or other problems.

As computerized tomography (CT scan) and magnetic resonance imaging (MRI) technologies are often able to provide improved imaging of the sinuses, the use of these scans may replace sinus x-rays in certain circumstances. Other related procedures that may be used to evaluate problems of the sinuses include x-rays of the skull, CT scan of the brain, and MRI of the brain and spine. Please see these procedures for more information. E. Computed Tomography (Also called CT or CAT scan.) A diagnostic imaging procedure that uses a combination of x-rays and computer technology to produce cross-sectional images (often called slices), both horizontally and vertically, of the body. A CT scan shows detailed images of any part of the body, including the bones, muscles, fat, and organs. CT scans are more detailed than general x-rays. F. Cultures from the Sinuses Laboratory tests that involve the growing of bacteria or other microorganisms to aid in diagnosis.

SINUSITIS Sinusitis is an infection of the sinuses near the nose. These infections usually occur after a cold or after an allergic inflammation. There are four types of sinusitis: • • •

•

Acute - symptoms of this type of infection last less than four weeks and get better with the appropriate treatment. Subacute - this type of infection does not get better with treatment initially, and symptoms last four to eight weeks. Chronic - this type of infection happens with repeated acute infections or with previous infections that were inadequately treated. These symptoms last eight weeks or longer. Recurrent - three or more episodes of acute sinusitis a year.

Causes of Sinusitis Sometimes, a sinus infection happens after an upper respiratory infection (URI) or common cold. The URI causes inflammation of the nasal passages that can block the opening of the paranasal sinuses, and result in a sinus infection. Allergies can also lead to sinusitis because of the swelling of the nasal tissue and increased production of mucus. There are other possible conditions that can block the normal flow of secretions out of the sinuses and can lead to sinusitis including the following: •

abnormalities in the structure of the nose

• • • • • • • •

enlarged adenoids diving and swimming infections from a tooth trauma to the nose foreign objects stuck in the nose cleft palate gastroesophageal reflux disease (GERD) secondhand smoke

When the flow of secretions from the sinuses is blocked, bacteria may begin to grow. This leads to a sinus infection, or sinusitis. The most common bacteria that cause sinusitis include the following: • • •

Streptococcus pneumonia Haemophilus influenzae Moraxella catarrhalis

Symptoms of Sinusitis The symptoms of sinusitis depend greatly on the age of the child. The following are the most common symptoms of sinusitis. However, each child may experience symptoms differently. Symptoms may include: Younger Children: •

• • • •

runny nose o lasts longer than seven to 10 days o discharge is usually thick green or yellow, but can be clear nighttime cough occasional daytime cough swelling around the eyes usually no headaches younger than 5 years of age

Older children and adults: • • • • • • • • •

runny nose or cold symptoms lasting longer than seven to 10 days drip in the throat from the nose headaches facial discomfort bad breath cough fever sore throat swelling around the eye, often worse in the morning

The symptoms of sinusitis may resemble other conditions or medical problems. Always consult your child's physician for a diagnosis. Treatment

Specific treatment for sinusitis will be determined by your child's physician based on: • • • • •

your child's age, overall health, and medical history extent of the infection your child's tolerance for specific medications, procedures, or therapies expectations for the course of the infection your opinion or preference

Treatment of sinusitis may include the following: • • • • • • • •

antibiotics, as determined by your child's physician (antibiotics are usually given for at least 14 days) acetaminophen (for pain or discomfort) a decongestant (i.e., pseudoephedrine [Sudafed®]) and/or mucus thinner (i.e., guaifenesin [Robitussin®]) cool humidifier in your child's room nasal spray (to reduce inflammation) medications to treat GERD surgery to remove the adenoids endoscopic sinus surgery

Antibiotics may be withheld for 10 to 14 days, unless severe symptoms develop, such as: fever, facial pain or tenderness, or swelling around the eye. Surgery should be considered only if other treatments have failed. Referral to an allergist/immunologist is often needed, particularly for people with chronic or recurrent sinusitis and for patients who have had sinus surgery, but still experience sinusitis. Antihistamines do not help the symptoms of sinusitis unless an allergy is involved. RHINITIS Rhinitis is a reaction that occurs in the eyes, nose and throat when airborne irritants (allergens) trigger the release of histamine. Histamine causes inflammation and fluid production in the fragile linings of nasal passages, sinuses, and eyelids. The two categories of rhinitis are: •

Allergic Rhinitis There are two types of allergic rhinitis: o o

Seasonal - occurs particularly during pollen seasons Perennial - occurs throughout the year

The most-common causes of allergic rhinitis are:

o o o o

pollen dust mites mold animal dander

Reactions from allergic rhinitis include: o o o o

sneezing congestion runny nose itchy nose, throat, eyes, and ears

Preventive measures for avoiding allergic rhinitis include: o

environmental controls, such as air conditioning, during pollen season

o

avoiding areas where there is heavy dust, mites, molds

o

avoiding pets

Treatments for allergic rhinitis, as determined by your physician and based on your condition, may include: o o o o •

oral medications inhaled medications immunotherapy allergy injections

Nonallergic Rhinitis Types of nonallergic rhinitis are: o

vasomotor rhinitis (irritant rhinitis)

o

eosinophilic

o

rhinitis medicamentosa

o

neutrophilic rhinosinusitis

o

structural rhinitis

o

nasal polyps

o

primary vasomotor instability

Causes of nonallergic rhinitis include:

o o o o o o

fumes odors temperature atmospheric changes smoke other irritants

Reactions from nonallergic rhinitis include: o o o o

sneezing congestion runny nose itchy nose, throat, eyes, and ears

The preventive measure for avoiding nonallergic rhinitis is avoiding the primary cause. Treatments for nonallergic rhinitis, as determined by your physician and based on your condition, may include: o o o o o

oral medications inhaled medications immunotherapy allergy injections surgery for some conditions

TONSILO-PHARYNEAL Anatomy and Physiology Tonsils Tonsils are clusters of lymphatic tissue just under the mucous membranes that line the nose, mouth, and throat (pharynx). There are three groups of tonsils. The pharyngeal tonsils are located near the opening of the nasal cavity into the pharynx. When these tonsils become enlarged they may interfere with breathing and are called adenoids. The palatine tonsils are the ones that are located near the opening of the oral cavity into the pharynx. Lingual tonsils are located on the posterior surface of the tongue, which also places them near the opening of the oral cavity into the pharynx. Lymphocytes and macrophages in the tonsils provide protection against harmful substances and pathogens that may enter the body through the nose or mouth. Tonsils are lymphoepithelial organs at the opening of the upper aerodigestive tract. From above downwards, they can be divided into:

1. pharyngeal tonsil, adenoid, which lies on the roof and posterior wall of the nasopharynx 2. tubal tonsil which lies around the eustachain tube 3. palatine tonsil which lies between the anterior and posterior faucial pillars 4. lingual tonsil which lies at the base of the tongue These lymphoid organs developed from the epithelium of the primitive oronasal cavity, the mesenchymal stroma and lymphoid cells then infiltrate these areas. Although the tonsils are present at embryonal stage, they only acquire their typical structure in the postnatal period. They begin increasing rapidly in size between the first and third year of life, with peaks in the third and seventh year. They involute slowly at early puberty. In contrast to other lymphoid aggregates, tonsils do not filter lymph. The palatine tonsil is supplied by the facial artery, ascending pharyngeal artery, lingual artery and the maxillary artery. Venous drainage is by the lingual and pharyngeal veins. Immunology Tonsils are composed primarily of B-lymphocytes. T-cell lymphocytes constitute 40% of total volume in contrast to 70% in circulating plasma. According to present knowledge, tonsils are involved in production of antibodies, interferon-gamma and lymphokines and in inducing secretory immunity.

Pharynx The pharynx is a tubular structure extending from the base of the skull to the esophageal inlet. Superiorly, it opens into the nasal and oral cavities; inferiorly, it opens into the larynx and the esophagus. It is lined with mucous membrane. The adenoids are located in the nasopharynx, the palatine tonsils in the pharynx, and the lingual tonsils in the hypopharynx; all are lymphoid tissue. The pharynx is subdivided into the nasopharynx, the oropharynx, and the hypopharynx.

Nasopharynx. The nasopharynx extends from the posterior choanae to the inferior surface of the soft palate. Malignancies of the nasopharynx can present as nasal obstruction, epistaxis, tinnitus, headache, diminished hearing, and facial pain. Oropharynx. The oropharynx extends from the junction of the hard and soft palates and the circumvallate papillae to the valleculae. It includes the soft palate and uvula, the base of the tongue, the pharyngoepiglottic and glossoepiglottic folds, the palatine arch (which includes the tonsils and the tonsillar fossae and pillars), the valleculae, and the lateral and posterior oropharyngeal walls. Carcinomas of the oro pharynx can present as pain, sore throat, dysphagia, and referred otalgia. Hypopharynx. The hypopharynx extends from the superior border of the hyoid bone to the inferior border of the cricoid cartilage. It includes the pyriform sinuses, the hypopharyngeal walls, and the postcricoid region (i.e., the area of the pharyngoesophageal junction). Malignancies of the hypopharynx can present as odynophagia, dysphagia, hoarseness, referred otalgia, and excessive salivation.

The pharynx is the region of the tonsils, back part of the nose and swallowing area. It is probably the most examined of all body regions, and reflects many diseases. Assessment To inspect the pharynx, the examiner asks the person to open the mouth without protruding the tongue. A tongue blade is pressed firmly down on the midpoint of the arched tongue; pressing farther back may cause gagging. The person then says “ah” while breathing through the mouth to prevent gagging. The oropharynx, that portion of the pharynx directly posterior to the oral cavity bounded by the nasopharynx above and laryngopharynx below, is examined with a tongue blade and a mirror. The anterior and posterior tonsillar pillars, the uvula, tonsils and posterior pharynx are inspected for color, symmetry, evidence of exudates, edema, ulceration, and tonsillar enlargement. Redness and swelling of the tonsils, pillars and uvula with white or yellow exudates on the tonsils may indicate streptococcal infection. Tonsils may be enlarged without being infected.

Examination of oral cavity should be done properly. Very often, the size of tonsils may be exaggerated during gagging and pressing hard with the use of a tongue depressor. The proper way is to gently place the tongue depressor anterior to the circumvallate papillae or if possible, just by inspection without the use of tongue depressor. The size and percentage of the obstruction should be recorded using the scale 0 to +4. 0 means the tonsil is in the fossa; +1 means less than 25% obstruction; +2 is less than 50%; +3 is less than 75% and +4 is more than 75% obstruction. Examination of the Pharynx for Problems

The pharynx can be seen partially by forceful traction on the tongue, by the fingers wrapped in a handkerchief. It begins in back of the one-half inch uvula, which hangs down freely from the posterior rim of the palate. 1. Observe the sides of the pharynx where the tongue appears to originate, and note the irregular flesh colored tonsils on each side. When removed, a small cavity remains in their site. Adult tonsils may be atrophied to a pea size or if irritated and infected, be as large as grapes and flecked with pus. 2. With a flashlight, examine the back of the pharynx while attempting to yawn. An allover redness, with noticeable soreness, usually means pharyngitis as in colds, sore throats, etc. 3. Examine the wall of the pharynx on all sides and the back of the tongue, if possible, for any one particular sore, ulcer or bleeding point, which may mean cancer. Diagnostic Procedures for the Tonsils and Pharynx A. Indirect Laryngoscopy Indirect laryngoscopy has been used since the 1800s for visualizing the pharynx and larynx. In this technique, the head light source illuminates the mirror, which in turn illuminates the laryngopharynx. The patient is seated in the sniffing position and protrudes the tongue while a warmed laryngeal mirror is introduced firmly against the soft palate in the midline to elevate the uvula out of the field (gently, so as not to elicit the gag reflex). The image seen on the mirror can be used to assess vocal cord mobility, as well as to inspect for a mass or foreign body of the larynx or pharynx. This technique can be performed rapidly and is inexpensive. B. Flexible Rhinolaryngoscopy Flexible rhinolaryngoscopy is currently one of the most commonly used techniques for visualizing the nasal cavity, the sinuses, the pharynx, and the larynx. The technique utilizes a small-caliber flexible endoscope and can be performed in an office setting. Before the procedure, the patient's nasal cavity is decongested and anesthetized for maximum visualization and minimal discomfort. In the procedure, the examiner threads the end of the scope into the nasal aperture along the floor of the nasal cavity. As the scope is advanced, the examiner can visualize the nasal cavity proper for any

evidence of lesions or masses. Once the scope approaches the nasopharynx, it is directed inferiorly and advanced slowly, allowing direct visualization of the entire pharynx and larynx. C. Direct Laryngoscopy Direct laryngoscopy has the advantage of permitting both diagnostic and therapeutic intervention. It is performed with the patient under general anesthesia and intubated. The procedure allows for direct visualization of the pharynx and the larynx and permits the surgeon to perform biopsies and remove small lesions. At the same time, the surgeon has the opportunity to palpate the structures of the oral cavity, the oropharynx, and the hypo pharynx, which cannot be properly palpated in an awake patient. The laryngoscope can also be suspended from a table-mounted Mayo stand (for hands-free use), and a microscope can be maneuvered into focal distance to allow magnified visualization of the glottis and subglottis. During a microscopic direct laryngoscopy, small lesions or topographic abnormalities can be better characterized and removed if desired. Some examples of lesions that can be diagnosed by direct laryngoscopy are vocal cord polyps, leukoplakia, intubation granulomas, contact ulcers, webs, nodules, hematomas, and papillomatosis. Additionally, small malignant lesions of the vocal cords can be examined and ablated or extirpated by using a CO2 laser under direct microlaryngoscopic guidance. D. Angiography Angiography is a widely used examination in which radiopaque dye is injected into the vessels by means of transcutaneous catheter insertion. It visualizes the internal wall and caliber of the vessel lumen, as well as the position of the vessel, which is usefl for the evaluation of certain parapharyngeal masses. Biopsy Procedures A. Fine-needle Aspiration FNA is often used to make an initial tissue diagnosis of a neck mass. The advantages of this technique include high sensitivity and specificity; however, 5% to 17% of FNAs are nondiagnostic. Another advantage of FNA is speed: If a cytologist or a pathologist is available, diagnosis can often be made within minutes of the biopsy. FNA is performed with a 10 ml syringe with an attached 21- to 25-gauge needle. Larger needles are more likely to result in tumor seeding. The patient is positioned to allow for optimal palpation of the mass. The skin overlying the mass is prepared with a sterile alcohol prep sponge. Local anesthesia is not necessary. The mass is grasped and held in a fixed and stable position. The needle is introduced just under the skin surface. As the needle is advanced, the plunger of the syringe is pulled back, to create suction. Once the mass is entered, multiple passes are made without exiting the skin surface; this maneuver is critical in maximizing specimen yield. After the final pass is completed, the suction on the syringe is released and the needle withdrawn from the skin. If a cyst is encountered, it should be completely evacuated and the fluid sent for cytologic analysis.

A drop of aspirated fluid is placed on a glass slide. A smear is made by laying another glass slide on top of the drop of fluid and pulling the slides apart to spread the fluid. Fixative spray is then applied. Alternatively, wet smears are placed in 95% ethyl alcohol and treated with the Papanicolaou technique and stains. FNA has several advantages over excisional biopsy. An FNA requires only an office visit, with minimal loss of time from work for the patient. In contrast, excisional biopsy is commonly performed in an operating room, so the patient must undergo preoperative testing. Patients with a significant medical history may require formal medical clearance. An excisional biopsy exposes the patient to the risks of anesthesia, postoperative wound infection, and tumor seeding. B. Ultrasound-Guided FNA Ultrasonographic guidance of FNA enables the surgeon to obtain a cytologic specimen of deeper or nonpalpable masses that are not amenable to standard FNA. Real-time imaging of the needle's passage allows the surgeon to plot a more accurate trajectory and avoid underlying vital structures. Furthermore, it provides an image of the mass, allowing its characterization as solid, cystic, or heterogeneous. With cystic or complex masses, it is imperative to place the tip of the needle into the wall to increase specimen yield. C. CT-Guided FNA CT-guided FNA is most commonly employed to diagnose poorly accessible or deep-seated lesions of the head and neck. Like ultrasound-guided FNA, CT-guided FNA provides visualization of the needle as it is passed through the tissue and into the underlying structures, thus allowing a more accurate needle trajectory and avoidance of underlying vital structures. Additionally, visual guidance of the needle greatly increases the likelihood of obtaining a specimen from the mass rather than the surrounding tissues. Imaging Procedures Because many of the deep structures of the head and neck are inaccessible to either direct evaluation by palpation or indirect evaluation via endoscopy, further information must be obtained by radiography. Imaging procedures such as CT, MRI, ultrasound, and positron emission tomography (PET) scanning permit the diagnosis and analysis of pathologic conditions affecting these deep structures, including the temporal bone, skull base, paranasal sinuses, soft tissues of the neck, and larynx. A. Ultrasonography Ultrasonography is a safe and inexpensive method of gaining high-resolution real-time images of the structures of the head and neck. Palpable masses in the neck can be assessed for changes in size, for association with other local structures, and for character (i.e., solid, cystic, or complex). Applications of ultrasonography include assessment of masses such as thyroglossal duct cysts, branchial cleft cysts, cystic hygromas, salivary gland tumors, abscesses, carotid body tumors, vascular tumors, and thyroid masses. Additionally, ultrasonography combined with FNA and cytologic

evaluation can provide both a detailed visual description and an accurate cytologic evaluation of masses in the neck. B. Computed Tomography A CT scan with intravenous contrast is often the first-line imaging technique used to evaluate a mass of the neck and to assess for pathologic adenopathy. CT has proved to be an effective method for primary staging of tumors and lymph nodes. Additionally, it has been shown to be effective in studying capsular penetration and extranodal extension. It is clearly superior to MRI in evaluating bone cortex erosion, given that MRI cannot assess bone cortex status at all. CT scans are also widely used for posttreatment surveillance in cancer patients. C. Magneic Resonance Imaging MRI avoids exposing the patient to radiation and provides the investigator with superior definition of soft tissue. For example, MRI can differentiate mucous membrane from tumor, as well as detect neoplastic invasion of bone marrow. In patients with nasal cavity tumors, MRI can distinguish between neoplastic, inflammatory, and obstructive processes. MRI is also valuable in assessing the superior extent of metastatic cervical lymphadenopathy (i.e., intracranial extension). A disadvantage of MRI is its limited ability to show bone detail; it therefore cannot detect invasion of bone cortex by a neoplasm. Furthermore, an MRI scan is significantly more expensive than a CT scan. D. Positron Emission Tomography PET scanning is a functional imaging technique that measures tissue metabolic activity through the use of radioisotopically tagged cellular building blocks, such as glucose precursors. A range of physiologic tracers has been developed for PET imaging, with the glucose analogue 2-deoxy-2-[(18)F]fluoro-D-glucose (FDG) the most commonly used. FDG has a half-life of 110 minutes. Once given to the patient, FDG is taken up by glucose transporters and is phosphorylated by hexokinase to become FDG-6-phosphate (FDG-6-P). Further metabolism of FDG-6-P is blocked by the presence of an extra hydroxyl moiety, which allows FDG-6-P to accumulate in the cell and serve as a marker for glucose metabolism and utilization. Because neoplastic cells have higher rates of glycolysis, localized areas of increased cellular activity on PET scans may represent neoplastic tissue. In this respect, PET is very different from CT and MRI, which depict tissue structure rather than tissue metabolic activity. Because FDG is nonspecifically accumulated in glycolytically active cells, it demarcates areas of inflammation as well as neoplastic tissue, which can lead to a false positive scan. Muscular activity during the scan can also lead to areas of increased uptake in nonneoplastic tissue. Furthermore, healing bone, foreign body granulomas, and paranasal sinus inflammation can produce false positive results. False negative scans occur when tumor deposits are very small (i.e., 3 to 4 mm or less in diameter). Thus, micrometastases are not reliably detected using an FDG-PET

image. Furthermore, a false negative scan can occur if the PET scan is performed too soon after radiation therapy. The role of PET imaging in head and neck oncology is rapidly expanding. Currently, the majority of PET imaging used in head and neck oncology is FDG based. FDG-PET is actively being used to look for unknown primary lesions and second primaries, to stage disease before therapy, to detect residual or recurrent disease after surgery or radiation therapy, to assess the response to organ preservation therapy, and to detect distant metastases. Because false positive and false negative PET scans do occur, accurate interpretation of PET scans requires a thorough understanding of the potential confounding factors. E. PET/CT PET/CT is essentially an FDG-PET scan that has been coregistered with a simultaneous CT scan to allow the radiologist to precisely correlate the area of increased cellular activity with the anatomic structure. This technique removes some of the guesswork involved with interpreting an area of increased activity on a simple PET scan and provides the physician with a morphologic correlate for the area of increased uptake. After a histologic diagnosis has been made and correlated with the imaging information, the patient and physician can have a comprehensive discussion of the pathology, the stage of the disease, and the selection of therapy.

NOSE DISORDERS EPISTAXIS Epistaxis is bleeding from the nose caused by irritation, trauma, coagulation disorders, hypertension, chronic infection or tumor. Epistaxis is thought to have occurred at least once in over 10 % of the normal population. It is either a primary disorder or secondary to another condition such as hemophilia or leukemia and many cases are idiopathic. In children, who are twice as likely to have epistaxis as adults, the bleeding is usually mild and tends to originate from the posterior septum so that the bleeding point is more difficult to locate and the bleeding may be profuse. Epistaxis is equally common in men and in women. Although epistaxis is a frightening experience for the patient, it generally looks and feels worse than it actually is. The blood is usually briught red and the patient may swallow some of it, which is an unpleasant sensation. Although adults can lose up to 1 L per hour during severe bleeding, the mortality is extremely low. When the patient bleeds enough to show signs of shock, the nosebleed usually stops because of low blood pressure; some deaths are thought to have been causes by coronary ischemia from blood loss. PATHOPHYSIOLOGY The most common cause of epistaxis is trauma to the nasal mucosa from damage by a foreign object, picking crusts from the nasal septum, or dryness of the

nasal mucosa. Nosebleeds are fairly common in patients with coagulation defects such as hemophilia, leukemia and purpura. Infection, tumors and some drugs and toxins may cause nosebleeds; in many instances however, the cause is simply not identified or is considered idiopathic. There may be some relationship between the menstruation and epistaxis. It may be that in some women with premenstrual syndrome the nasal mucosa becomes congested at the time of menstruation, setting the stage for epistaxis. The incidence of epistaxis is no higher in hypertensive patients than in normotensive patients. However, hypertensive patients may bleed more profusely, partly because of the direct effect of the increased pressure and also because the small nasal arteries and arterioles of hypertensive patients tend to have much of their muscular walls replaced by fibrous tissue and are incapable of contracting adequately to attain hemostasis. Children experience frequent nosebleeds from the anteroinferior part of the septum known as the Little’s area or Kiesselbach’s plexus. The etiology is not clear, but the area is richly vascular and children have hyperemic and congested upper respiratory tracts. Children also pick up and rub their noses in the area where the mucosa is stretched over the cartilage and bone. Intractable nose picking is another cause of anterior nosebleeds. Some patients cannot stop picking their noses, either because of a nervous habit or because crusts are present from an earlier ulceration or perforation. Constant nose picking can cause septal ulceration or even a perforation which leads to epistaxis. A hereditary disease that is an unusual cause of epistaxis is Rendu-Osler-Weber disease of hemorrhagic hereditary telangiectasia. This disease is gene dominant and may be passed from either parent to a child of either sex. Epistaxis is usually the initial symptom, but telangiectasis is commonly found in other mucous membranes or anywhere on the external surface of the body. Bleeding usually occurs from the nose and gastrointestinal tract because mucosa in those areas is very fragile, whereas other areas have protective layers of squamous epithelium. Most nosebleeds in the anterior part of the nose originate from Kiesselbach’s plexus, the highly vascular network in the anterior septum. It is also anatomically closer to the rapid inspiratory air flow, which may dry the normal mucus flow especially in cold, dry weather. Because the vessels are fairly small and easily accessible, these nosebleeds are the easiest to treat. If the bleeding is from the posterior part of the nose, the exact source of bleeding is more difficult to locate because it is sometimes impossible to see and bleeding is more profuse. Usually just one source on one side of the nose bleeds, although bleeding frequently originates from both sides in patients with blood dyscrasias. Diagnostic Studies and Findings • Hematocrit • Hemoglobin • Platelets • Prothrombin time • Partial thromboplastin time • Reticulocyte count and differential - done to rule out coagulation defect, results usually normal; bleeding from other parts of body likely in patients with hematologic disorders. • Rhinoscopy • Nasopharyngoscopy

-

to detect and localize site of planning

Medical and Surgical Management 1. Arterial ligation of ethmoid, maxillary or carotid artery if proper packing fails to control nosebleed. > an incision is made I the gumline above the incisor on the affected side, and the maxillary sinus is entered. The artery that supplies the area of bleeding is identified, and a metal clip or suture is used to ligate the artery. 2. Endoscopic cautery – chemical or electrical cauterization of bleeding vessels using nasal endoscope to visualize bleeding.

3. Septal dermoplasty for Rendu-Osler-Weber disease

- skin graft is placed in nose to cover anterior parts of septum and floor and walls of nose anteriorly to provide protective covering over fragile mucosa; combined with laser therapy gains control of epistaxis for several years.

4. For anterior bleeding:

 Anterior nasal packing may be all that is required. Antibacterial ointment such as Bacitracin or Neosporin is applied to half inch gauze and gently, but firmly inserted into the anterior nasal cavities to apply pressure to the bleeding vessels  Nasal packing should be in place for a minimum of 48 to 72 hours. For posterior plugs:

Figure 4. Posterior nasal packing. A. After adequate anesthesia has been obtained, a catheter is passed through the affected nostril and through the nasopharynx, and drawn out the mouth with the aid of ring forceps. B. A gauze pack is secured to the end of the catheter using umbilical tape or suture material, with long tails left to protrude from the mouth. C. The gauze pack is guided through the mouth and around the soft palate using a combination of careful traction on the catheter and pushing with a gloved finger. This is the most uncomfortable (and most dangerous) part of the procedure; it should be completed smoothly and with the aid of a bite block (not shown) to protect the physician's finger. D. The gauze pack should come to rest in the posterior nasal cavity. It is secured in position by maintaining tension on

the catheter with a padded clamp or firm gauze roll placed anterior to the nostril. The ties protruding from the mouth, which will be used to remove the pack, are taped to the patient's cheek.  A small, red rubber catheter is passed through the nose into the oropharynx and mouth. A small gauze pack is tied to the catheter, and it is withdrawn; this moves the pack into proper placement in the nasophrarynx and posterior nose to apply pressure.  The nasal cavity is packed with half-inch gauze and the strings from the posterior pack are tied around a rolled gauze for maintaining its position. The ties from the oral cavity are taped to the client’s face in order to prevent loosening or dislodgement of the plug.  General comfort measures such as humidification, the use of drip pad to collect bloody drainage and mucus, and providing lubrication to the nares.  Nurse must monitor for bleeding, and the proper placement of the posterior plug. If the plug is visible in the oral cavity, notify the physician for readjustment of the packing.  Posterior nasal packs should be in place for 5 days.  Prophylactic antibiotics are administered to prevent toxic shock syndrome and sinusitis. 5. Balloon pressure catheter tubes  stents look like very short ( about 6 inches) urinary catheters. These tubes have an exterior balloon along the tube length in addition to an anchoring balloon on the end. These tubes are inserted into both nares. The physician first inflates the anchoring balloon to keep the tubes in place. Then the pressure balloons are inflated carefully for both tubes at the same time to compress bleeding vessels. Placement of posterior packing or pressure tubes is uncomfortable and airway may be obstructed.  Nurse should observe for respiratory distress and tolerance of the tubes. Pain medication may be prescribed. Oral care and adequate hydration are important because of mouth breathing.  The tubes are usually removed after 2-5 days; teach the client measures for comfort and safety. Like the use of petroleum jelly for lubrication, nasal saline sprays and humidification. Instruct the client to avoid vigorous nose blowing, use of aspirin and other NSAIDS, and strenuous activities. Medications: • Fibrinolytics VITAMIN K (Aquamephyton) 10mg po or IM; useful in some cases of epistaxis, but packing remains therapy of choice • Anti-infective agents PENICILLIN 1.5 million U, IV q6h recommended for prophylaxis because packing obstructs drainage of paranasal sinuses and may precipitate a sinus infection. Nursing Assessment/ Interventions 1. Assess for: Nasal Bleeding Bright red blood comes from the nares; patient may also swallow or expectorate blood; history of trauma, nose picking or other unknown cause.

2. Examination of patient’s body for bruises or petechiae that may indicate underlying hematologic disorder. 3. Nursing Diagnoses: • Risk for fluid volume deficit r/t nasal bleeding • Fear r/t loss of blood • Risk for aspiration r/t inability to clear secretions; gagging • Altered cerebral and cardiopulmonary tissue perfusion r/t largevolume blood loss 4. Interventions for: ANTERIOR BLEEDING  Assess the location of bleeding  Pinch the nose firmly and hold for at least 10 minutes. It is best if you pinch the patient’s nose instead of asking the patient to do so. This way, you can ensure steady and firm pinching.  If bleeding continues beyond the pinching 10 min. period, prepare the client for additional treatment.  With the patient in a high Fowler’s position, slightly hyper flex the head and suction the clots in the nasal passage.  Observe the canal for continued bleeding. If present, apply vasoconstriction agent such as 10% cocaine solution.  If bleeding continues, the nose may need to be cauterized with silver nitrate or anterior nasal packing inserted. POSTERIOR BLEEDING The bleeding usually originates from the sphenopalatine artery, anterior ethmoid artery or the nasopalatine artery.  Assess that the bleeding is posterior.  Place the patient in a high Fowler position.  As ordered, anesthetize the posterior nasal passage with 10% cocaine solution  Pack the bleeding site with packing materials such epistaxis catheter, Foley catheter tip and or tampon.  Monitor vital signs and estimate blood loss. If necessary, provide fluid volume replacement  Instruct patient to (1) tilt head forward if bleeding occurs (2) not to blow nose and (3) to apply steady pressure for at least 5 min. if bleeding recurs. NASAL FRACTURES A nasal fracture is a traumatic injury to the nasal bones. Most common causes are accidents, sports injuries, and assaults. In children, falls are the most common cause of nasal fractures. They occur more commonly in men, however when nasal fractures are diagnosed, it is essential to rule out fractures of the associated facial bones such zygomatic or mandibular fractures because facial injuries or trauma may also damage \these bones. Even a nasal fractures that appear simple usually have associated damage to the mucosal lining of the nose. If the patient suffered a facial trauma that causes epistaxis, damage to the bone-cartilage structures of the nose is more likely.

PATHOPHYSIOLOGY A nasal fracture occasionally occurs in the birth canal during delivery. These are usually “greenstick” fractures, and the baby’s nose inclines slightly to one side. The nose can be grasped at the tip and pulled toward the midline to realign it. Nasal fractures can be classified as unilateral, bilateral or complex. Unilateral fracture – may produce little no displacement and may appear on an xray examination as a simple crack. Bilateral fractures – which are the most common, may be caused by a swinging punch or blow that pushes both nasal bones to one side or by a frontal blow that depresses the nasal bones and gives a flattened look to the nose. The entire nose may be deviated and the nose may have a C or S deformity. Complex fractures – are usually caused by a powerful frontal blow. Such blows may shatter the nasal pyramid and frequently the frontal bones as well, causing a marked depression of the nasal and frontal bones. The usual findings are epistaxis, a noticeable facial deformity and a history of trauma. Edema occurs quickly at the injury site and depending on the severity may include a periorbital swelling. Ecchymosis is common, the nose is exquisitely tender, and nasal obstruction occurs. Complex fractures of the nose and face may result in diplopia and subscleral hemorrhage. Diagnostic Studies and Findings: •

X-ray examination of the face and nose – shows fractures and depressed areas of facial and nasal bones; done to complement clinical, visual evaluation. • Ophthalmoscopy – performed to rule out eye injury such as corneal abrasion or laceration, also to check lacrimal apparatus and orbit.  Medical and Surgical Management

1. Reduction and Fixation of the fractures as quickly as possible after injury (within first hour or two before swelling beings, or after 3 or 4 days when swelling has decreased) because fragments tend to stabilize quickly; bilateral nasal packing or nasal splints usually inserted during surgery to maintain stability and position of nasal structure.

2. Rhinoplasty – is a surgical reconstruction of the nose for cosmetic purposes and to improve airflow. The client returns from surgery with packing on both nostrils; the gauze packing is usually treated with antibiotic to reduce risk for infection. A “moustache” dressing (or drip pad) often a folded 2x2 gauze pad is usually placed under the nose. A splint or cast may cover the nose for additional alignment and protection. After surgery: • Observe for edema and bleeding.check v/s q4. the client with uncomplicated rhinoplasty may be discharge the day of surgery. • Place the patient in a semi-Fowler’s postion and instruct to move slowly

• • • •

Apply cool compresses to nose, eyes or face to reduce swelling and bruising. To prevent bleeding, instruct patient to limit Valsava maneuvers for the first few days after packing is removed. Laxatives or stool softeners may be prescribed to ease bowel movement. Instruct client to avoid aspirin and NSAIDS to prevent bleeding. Explain that edema and discoloration may last for weeks and the final surgical result will be evident in 6 to 12 months.

3. Medications: Narcotic analgesics or antipyretics •

3.

Acetaminophen (TYLENOL), 325-650 mg with/without codeine po q4-q6 prn

General Management: Simple thumb pressure on convex side of the nose occasionally enough to push bones back together.

Nursing Assessment/ Interventions 1. Assess for: Facial swelling; deformity; ecchymosis; epistaxis; nose very tender; history of trauma to face and nose; possible accompanying lacerations; leak of CSF fluid, a clear fluid dripping from then nose and/or ears. Respiratory Status; difficulty in breathing through the nose; mouth breathing 2. Nursing Diagnoses and Interventions: • PAIN r/t facial trauma Assess need for pain medication and provide adequate analgesia for pain relief; evaluate and document effectiveness. •

• •

INEFFECTIVE BREATHING PATTERN r/t nasal obstruction and swelling - Monitor vital signs and level of consciousness. - Assess for shortness of breath, dyspnea from nasal obstruction or difficulty in swallowing. - Apply ice to face and nose to minimize swelling and bleeding without pressure to nose. - Monitor amount and color of epistaxis and record - Keep head of bed elevated, even when sleeping to prevent aspiration of blood or secretions and minimize edema. - Prevent patient from swallowing blood or aspirating; encourage patient to breathe through mouth. - Have basin nearby for patient to expectorate blood. Provide frequent oral hygiene and encourage intake of oral fluids.

SENSORY/PERCEPTUAL ALTERATIONS (visual) r/t periorbital edema - Assess for eye swelling; apply ice to minimize edema - Observe for scleral hemorrhage and periobital edema - If eyes are not completely closed, assess patient’s ability to see.

NASAL POLYPS Polyps are benign grapelike cluster of mucous membrane and connective tissue growths that appear as soft, pale gray, non tender masses and gradually form from recurrent, localized swelling of the sinuses or nasal mucosa. Polyps are seen in about 90% of patients with chronic maxillary sinusitis. Polyps may become quite large. They are usually bilateral, occur in multiples and may cause actual distention and enlargement of bony structures of the nose. Even after surgical removal, some nasal polyps recur. Although rare in children, polyps are occasionally found in children with cystic fibrosis and allergies and in those with Peutz-Jeghers syndrome. The symptoms of this syndrome include pigmented spots on the skin, especially around the mouth and polyposis of the gastrointestinal tract. Many patients with polyps have anosmia or hyponosmia. PATHOPHYSIOLOGY The etiology of nasal polyps is not clear. They are often suspended in the nasal cavity by stalks of varying lengths. The polyps and stalks usually originate in the paranasal sinuses, particularly the ethmoid sinuses and pass into the middle meatus of the nose through the ostia connecting them to the nasal cavities. They are often called pseudotumors. Their pathogenesis is thought to be the result of focal mucosal edema that causes a polypoid swelling. Because of the polyp’s weight, the swelling tend to enlarge and eventually becomes suspended on a stalk. Polyps are usually found in the middle meatus near the openings of the sinuses and in the roof of the nose. They are never found on the septum or in the lower meatus; the reason for this is not known. Nasal polyps are often found in patients with allergy, cystic fibrosis, asthma, disorders of ciliary motility, chronic rhinitis and chronic sinusitis. The exact relationship is unknown but may be related to an inflammatory response causing hypertrophy of the mucosa, edema, and thinning of mucous membranes. An interesting phenomenon that occurs in some patients with asthma and nasal polyps is intolerance to aspirin, indomethacin and coal tar dyes. The intolerance is severe, and can cause respiratory arrest if these substances are ingested. This is thought to be related to the inhibitory action of these substances on prostaglandin synthesis. Diagnostic Studies and Findings:

• •

X-ray examination of sinuses. Shadows over affected areas ethmoid sinuses and sometimes maxillary sinuses appear opaque. Immunologic assessment. Performed if allergy is considered a causative effect.

Medical and Surgical Management

1. Polypectomy – each polyp avulsed with wire snare.

2. Caldwell-Luc procedure – may be performed if polyps originate in maxillary sinus.

3. Functional endoscopic sinus surgery – removal of polyps using nasal endoscope. Medications: • Corticosteroids. Prednisone high dose for 5 days. • Methyprednisolone – decreasing doses may be used for severe nasal obstruction to decrease size of polyps. • Steroids not recommended for long term use; steroid sprays may be used for long term control of the size of polyps and to prevent recurrence by reducing the inflammatory response. • Antihistamines • Decongestants • Anti infective agents Nursing Assessment: Nasal Obstruction; feeling of fullness in face or nose; nasal obstruction; difficulty in breathing through nose; nasal discharge; anosmia; symptoms of allergic rhinitis such as sneezing, watery eyes, eczema and asthma. Nursing Dx and Interventions: INEFFECTIVE AIRWAY CLEARANCE r/t swelling of the nasal mucosa and nasal obstruction • • •

• •

• • • •

Monitor patient’s vital signs. Assess patient’s ability to clear secretions, and amount of swelling. Increase humidification. After polypectomy, elevate head of bed and apply ice compresses to nose to minimize swelling and bleeding. Change nasal drip pad as indicated and record amount and consistency of drainage. Encourage patient not to swallow blood or secretions and expectorate into basin to prevent nausea. Instruct patient not to blow nose to prevent tissue trauma and promote healing. Observe for bleeding, and if bleeding occurs, instruct patient to notify physician, elevate head of bed, check vital signs, compress outside of nose against septum and apply ice compress to nose. If bleeding persists, packing may be necessary.

SENSORY/PERCEPTUAL ALTERATIONS (olfactory) r/t anosmia, presence of nasal edema •

Assess patient’s ability to smell.

• •

Assure patient that sense of smell should return postoperatively after swelling has decreased. Instruct patient to make appropriate adaptations to environment.

SEPTAL DEVIATION AND PERFORATION A deviated septum is a shift of the septum from the midline, which is common in many adults. It is either S or C shaped. Although the septum is usually straight at birth, it may shift from one side to another as a result of trauma or injury. A septal perforation is a hole in the nasal septum between the nostrils, which is usually in the anterior or cartilaginous septum but may occasionally occur in the bony septum. A small perforation, which can be caused by infections, nasal crusting, or nose picking is often asymptomatic, although a slight whistle may be heard as the patient breathes. Larger perforations may produce rhinitis, nasal crusting or epistaxis. PATHOPHYSIOLOGY The nasal septum, the dividing structure of the nose, is usually straight and divides the nose into two equal chambers. The septum is occasionally bent during birth, and the infant may have a twisted appearing nose. With aging, the septum has a tendency to become deviated or to form a hump. There is frequently no history of injury to account for the deviation. As a result, few adults have a totally straight septum. Trauma during childhood may also contribute to septal deviations in the adult. There is also a congenital disorder called choanal atresia, where the back of the nasal passage is blocked, usually by abnormal bony or soft tissue. It can be unilateral or bilateral. Sometimes, a unilateral choanal atresia is not detected until much later in life because the baby manages to get along with only one nostril available for breathing Septal perforations may be small or large. They may be asymptomatic or may cause annoying symptoms such as crusting, watery discharge, or a whistling noise as the patient breathes. Small perforations are usually caused by repeated irritation of the nose such as picking it: they may also be caused by septal surgery. Less frequent causes are repeated cauterization because of epistaxis, abuse of intranasal lidocaine, and chronic nasal infections. Ninety percent of perforations are in the anterior cartilaginous portions of the nose, less than 10% are in the posterior bony portions. Diagnostic Studies and Findings Facial X-ray examination, examination with nasal speculum or endoscope. - Show a shift of the septum or a perforation.

septal

Medical and Surgical Management For deviation: Submucous resection (SMR) – may be performed to reposition septum and relieve nasal obstruction

Rhinoplasty – may be done to correct nasal structure deformity Septoplasty – to replace septum in midline, may be done to relieve nasal obstruction and to enhance external appearance of nose. For perforation: Surgical closure – possible but not always successful; a Silastic “button” prosthesis may be inserted to close perforation. MEDICATIONS:

Analgesics Antihistamines Decongestants Antiinfective agents

General Management: • • •

Local application of lanolin or petroleum twice a day to prevent crusting Irrigate nose with normal saline or a dilute solution of sodium bicarbonate two or three times a day to keep the nasal mucosa hydrated (for perforations) Packing to control bleeding, if present. ( for deviation)

Nursing Assessment: Irregularities or deformity of external nose; obstruction to nasal breathing; feeling of facial fullness; headaches; epistaxis; crusting of nasal mucosa; whistle sound when breathing (perforation); or sinusitis Nursing Dx and Interventions: INEFFECTIVE BREATHING PATTERN r/t septal deformity causing obstruction • Assess and record respiratory status. • Postoperative care includes explanation in patient that facial and periorbital edema may be present and that nasal packing or nasal splints may be used. • Instruct patient to breathe though mouth during this time. IMPAIRED SKIN INTEGRITY r/t surgery on septum • Keep head of bed slightly elevated to prevent edema and promote drainage. • Use ice compresses on face to decrease edema, pain and bleeding. • Use cool mist vaporizer to assist in liquefying secretions. • Point out that patient may experience difficulty swallowing if nasal packing is used. • Change drip pad as necessary, recording color, consistency and amount of drainage. • Provide meticulous mouth care because patient is breathing through mouth. RISK FOR INJURY r/t bleeding or tissue trauma • Assess and report presence of excessive bleeding, swallowing or purulent discharge • Caution patient against attempting to blow nose, may cause bruising, edema and bleeding.

•

Caution patient not to smoke for at least 2 days; limit physical activity for several days to prevent irritation or trauma to tissues, which may cause bleeding.