MYOPIA

In myopia (nearsightedness) the light rays are focused in front of the retina. Myopia may occur because of excessive light refraction by the cornea or lens or because of an abnormally long eye. Myopia may also occur because of lens swelling, which occurs when blood glucose levels are elevated, as in uncontrolled diabetes. This type of myopia is transient and variable and fluctuates with the blood glucose level.⁴

HYPEROPIA

In hyperopia (farsightedness) the light rays focus behind the retina and the patient must use accommodation to focus the light rays on the retina for near and far objects. This type of refractive error occurs when the cornea or lens does not have adequate focusing power or when the eyeball is too short.

PRESBYOPIA

Presbyopia is the loss of accommodation associated with age. This condition generally appears at about age 45 years. As the eye ages, the crystalline lens becomes larger, firmer and less elastic. These changes, which progress with ageing, decrease the eye’s accommodative ability. People with presbyopia have difficulty focusing on near objects without some visual aid.⁵

ASTIGMATISM

Astigmatism is caused by an irregular corneal curvature. This irregularity causes the incoming light rays to be bent unequally. Consequently, the light rays do not come to a single point of focus on the retina. Astigmatism can occur in conjunction with any of the other refractive errors.

APHAKIA

Aphakia is defined as the absence of the crystalline lens. The lens may be absent congenitally or it may be removed during cataract surgery. A lens that is traumatically dislocated results in functional aphakia, although the lens remains in the eye. Since the lens accounts for approximately 30% of ocular refractive power, the absence of the lens results in a significant refractive error.⁶ Without the focusing ability of the lens, images are projected behind the retina.

NON-SURGICAL CORRECTIONS

Contact lenses

Contact lenses are another way to correct refractive errors. Contact lenses generally provide better vision than glasses because the patient has more normal peripheral vision without the distortion and obstruction of the glasses and their frames. Aphakic contact lenses magnify objects only approximately 7% and are visually superior to aphakic glasses.⁷ However, many older patients have difficulty handling and caring for contact lenses. Table 21-2 describes the various types of contact lenses and the advantages and disadvantages of each.

TABLE 21-2 Types of contact lenses

Lenses may be either rigid or flexible (soft lenses). Rigid contact lenses ride on the tear film layer of the cornea and are held in place by surface tension. Blinking causes the tear film to move under and over the contact lens, providing oxygen for the cornea. If the oxygen supply to the cornea is decreased, it becomes swollen, visual acuity decreases and the patient experiences severe discomfort.

Soft contact lenses do not ride on the corneal tear film layer so the cornea cannot receive oxygen from the tear film. Instead, the cornea receives oxygen through the soft contact lens, which is permeable to oxygen. Gas-permeable rigid contact lenses also allow oxygen to reach the cornea through the lens itself.

Altered or decreased tear formation can make wearing contact lenses difficult. Tear production can be decreased by antihistamines, decongestants, diuretics, oral contraceptives and hormones produced during pregnancy. Allergic conjunctivitis with itching, tearing and redness can also affect contact lens wear.

In general, the nurse must know whether the patient wears contact lenses, the pattern of wear (daily versus extended) and care practices. The nurse must be able to identify whether contact lenses are present and should know how to remove them in an emergency situation. Shining a light obliquely on the eyeball can help visualise a contact lens. A hard contact lens can be removed with a small suction cup designed for that purpose.

Patients should know the signs and symptoms of contact lens problems that must be managed by the eye care professional. They may remember these symptoms better if the nurse uses the mnemonic RSVP:

Redness

Sensitivity

Vision problems

Pain

The nurse must stress the importance of removing contact lenses immediately if any of these problems occur.

SURGICAL THERAPY

Surgical procedures are designed to eliminate or reduce the need for glasses or contact lenses and correct refractive errors by changing the focus of the eye. Surgical management for refractive errors includes laser, intraocular lens (IOL) implant and thermal procedures.

LEVELS OF VISION IMPAIRMENT

Patients may be categorised by the level of visual loss.¹³ Low vision is a form of vision impairment that involves irreversible vision loss. Low vision is significantly reduced vision but not blindness. The World Health Organization (WHO) defines low vision in two ways. From an epidemiological perspective, it is defined by measures of visual acuity and/or visual field, as when visual acuity is less than 6/18 and equal to or better than 3/60 in the better eye with best correction.^13,14 From a service provision perspective, low vision is defined in functional terms if a person has impairment of visual functioning even after treatment and/or standard refractive correction, and has a visual acuity of less than 6/18 to light perception, but uses, or is potentially able to use, vision for the planning and/or execution of a task.¹⁴ WHO estimates that there are 124 million people with low vision worldwide, 90% of whom live in developing countries.¹⁵

Legally blind is a term used in Australia to determine a person’s low vision level where there is no possibility of correcting vision through treatments such as surgery, laser or corrective glasses. Legally blind individuals can have some usable vision. The majority of people who are legally blind (i.e. have less than 6/60 vision in the better eye or a field of vision restricted to 20° in diameter or less, or a combination of both) will most likely be eligible to receive special benefits or services.^13,14 They may use vision substitutes, such as guide dogs and canes for ambulation and Braille for reading. Vision enhancement techniques (see below) are not usually helpful. Total blindness is defined as no light perception and no usable vision.

Partially sighted individuals who are not legally blind have a corrected visual acuity greater than 6/60 in the better eye and greater than 20° of visual field, but the visual acuity is 6/15 or worse in the better eye. Patients who are partially sighted can benefit greatly from visual assistive technology. Assistive technology refers to all equipment and technology, both hardware and software, that assists people to access or participate in a particular activity or range of activities. Examples of assistive technologies can be found on Vision Australia’s website (see Resources on p 506).

NURSING MANAGEMENT: VISION IMPAIRMENT

Nursing implementation

Health promotion

The nurse should encourage the partially sighted patient with preventable causes of further vision impairment to seek appropriate healthcare. For example, the patient with vision loss from glaucoma may prevent further visual impairment by complying with prescribed therapies and suggested ophthalmic evaluations.

Acute intervention

It is important to provide care that addresses the following major areas: environmental management, emotional support and family involvement. The nurse provides emotional support and direct care to the patient with recent visual impairment. Active listening and grief work facilitation are important components of nursing care for the recently visually impaired patient. The nurse should allow the patient to express anger and grief and should help the patient to identify their fears and successful coping strategies. The family is intimately involved in the experiences that follow vision loss. With the patient’s knowledge and permission, the nurse should include family members in discussions and encourage members to express their concerns.

Many people are uncomfortable around a blind or partially sighted individual because they are not sure what behaviours are appropriate. Sensitivity to the patient’s feelings without being overly solicitous or stifling the patient’s independence is vital in creating a therapeutic nursing presence. The nurse should always communicate in a normal conversational tone and manner with the patient, and should address the patient, not a family member or friend who may be with the patient. Common courtesy dictates introducing oneself and any other persons who approach the blind or partially sighted patient and saying goodbye on leaving. Making eye contact with the partially sighted patient accomplishes several objectives. It ensures that the nurse speaks while facing the patient so that the patient has no difficulty hearing the nurse. The nurse’s head position validates that the nurse is attentive to the patient. Also, establishing eye contact ensures that the nurse can observe the patient’s facial expressions and reactions.

The nurse should explain any activities or noises occurring in the patient’s immediate surroundings. Orientation to the environment lessens the patient’s anxiety or discomfort and facilitates independence. In orienting the partially sighted or blind patient to a new area, the nurse should identify one object as the focal point and describe the location of other objects in relation to it. For example, the nurse may say, ‘The bed is straight ahead, approximately 10 steps. The chair is to the left, and the nightstand is to the right, near the head of the bed. The bathroom is to the left of the foot of the bed.’

The nurse should assist the patient to each major object in the area, using the sighted-guide technique. When using this technique, the nurse stands slightly in front and to one side of the patient and offers an elbow for the patient to hold. The nurse serves as the sighted guide, walking slightly ahead of the patient with the patient holding the back of the nurse’s arm (see Fig 21-2). When using this technique in any situation, the nurse should describe the environment to help orient the patient. For example, the nurse may say, ‘We’re going through an open doorway and approaching two steps down. There is an obstacle on the left.’ To assist patients to sit, the nurse should place one of the patient’s hands on the back of the chair.

Figure 21-2 Sighted-guide technique. The nurse serves as the sighted guide, walking slightly ahead of the patient, with the patient holding the back of the nurse’s arm.

Ambulatory and home care

Rehabilitation after partial or total loss of vision can foster independence, self-esteem and productivity. The nurse should know what services and devices are available for the partially sighted or blind patient and should be prepared to make appropriate referrals for those services and devices. A list of agencies that serve partially sighted or blind patients in Australia is available from Vision Australia (see Resources on page 506). In New Zealand, the Royal New Zealand Foundation of the Blind assists people to maintain independence and lifestyle after vision loss by teaching them the safest techniques for moving around (see Resources on p 506).¹² Instructors in techniques of daily living teach clients how to undertake everyday tasks, such as cooking, eating, sorting laundry and getting money from an automatic teller machine. Other agencies are listed in the Resources on page 506.

Using Braille or audio books for reading and a cane or guide dog for ambulation are examples of vision substitution techniques. These are usually most appropriate for patients with no functional vision. For most patients who have some remaining vision, vision enhancement techniques can provide enough help for them to learn to ambulate, read printed material and accomplish activities of daily living.

Optical devices for vision enhancement

Telescopic lenses for near or far vision and magnifiers of various types can often enhance patients’ remaining vision enough for them to be able to perform many previously impossible tasks and activities. Most of these devices require some training and practice for successful use.¹⁶ Closed-circuit television can provide magnification up to 60 times, allowing some patients to read, write, use computers and do crafts. Although these systems are expensive and have limited portability, they are available in some public or university libraries.

Non-optical methods for vision enhancement

Approach magnification is a simple but sometimes overlooked technique for enhancing the patient’s residual vision. The nurse can recommend that the patient sit closer to the television or hold books closer to their eyes, which the patient may be reluctant to do unless encouraged. Contrast enhancement techniques include watching television in black and white, placing dark objects against a light background, or vice versa (e.g. a white plate on a black placemat), using a black felt-tip marker and using contrasting colours (e.g. a red stripe at the edge of steps or kerbs). Increased lighting can be provided by halogen lamps, direct sunlight or gooseneck lamps that can be aimed directly at the reading material or other near objects. Large type is often helpful, especially in conjunction with other optical or non-optical vision enhancements.

Gerontological considerations: visual impairment

The older patient is at an increased risk of vision loss because cataracts, glaucoma, diabetic retinopathy, macular degeneration and other potential causes of visual impairment are more common in older patients. This is particularly so for the Indigenous population of Australia. Older patients may have other deficits, such as cognitive impairment or limited mobility, which further affect the ability to function in usual ways. Societal devaluation of older people may compound the self-esteem or isolation issues associated with the older patient’s visual impairment. Financial resources may meet normal needs but can be inadequate in meeting increased demands associated with vision services or devices.

Older patients may become confused or disoriented when visually compromised. The combination of decreased vision and confusion increases the risk of falls, which have potentially serious consequences for the older adult. Decreased vision may compromise the older patient’s ability to function, causing concerns about maintaining independence and a decreased self-image. Decreased manual dexterity may make the instillation of prescribed eye drops difficult for some older adults.

HORDEOLUM

A hordeolum (commonly called a stye) is an infection of the sebaceous glands in the lid margin. The most common bacterial infective agent is Staphylococcus aureus.¹⁹ A red, swollen, circumscribed and acutely tender area develops rapidly. The nurse should instruct the patient to apply warm, moist compresses at least four times a day until it improves. This may be the only treatment necessary. If there is a tendency for recurrence, the patient should perform lid scrubs daily. In addition, appropriate antibiotic ointments or drops may be indicated.

CHALAZION

A chalazion is a swelling arising from a blockage of one or more meibomian ducts. It may affect either the upper or the lower lid. When it becomes infected it is sometimes called an internal hordeolum. It may also occur as a response to the material released into the lid when a blocked gland ruptures. A chalazion appears as a swollen, non-painful, reddened area, usually on the upper lid. It may fluctuate in size during the course of the condition and may reoccur several times. Initial treatment is similar to that for a hordeolum. If warm, moist compresses are ineffective in causing spontaneous drainage, the ophthalmologist may surgically remove the chronic lesion (this is normally a surgical procedure) or may inject the chronic lesion with corticosteroids.

BLEPHARITIS

Blepharitis is a common term used for inflammation of the lids, lashes and meibomian glands and is among the most common of ocular disorders.²⁰ It is usually chronic, with periods of exacerbation and remissions. It can be very difficult to treat. The pathology is complex and may involve abnormal lid-margin secretions and organisms, as well as a dysfunctional precorneal tear film.²¹ The general clinical features include sore eyelids; itchy, burning or gritty sensations; photophobia; and eyelids sticking together. Conjunctivitis may occur simultaneously.

The most common organisms seen in chronic blepharitis include Staphylococcus epidermidis, Staphylococcus aureus, Propionibacterium canes and Corynebacterium. Alterations in the secretions from the meibomian glands and changes to the orifices of the glands may occur in chronic blepharitis. Over time these changes result in instability and thinning of the tear film. This allows more of the aqueous component of tears to evaporate, ultimately leading to damage to the ocular surface and in dysfunctional tear syndrome. Treatment usually needs to be ongoing and is based on scrupulous eyelid hygiene, topical and systemic antibiotics and, in acute inflammatory periods, topical anti-inflammatory agents such as corticosteroids.²¹

CONJUNCTIVITIS

Conjunctivitis is an infection or inflammation of the conjunctiva and is one of the most common causes of red eyes. Conjunctival infections may be caused by bacterial or viral microorganisms. Conjunctival inflammation may result from exposure to allergens or chemical irritants (including cigarette smoke). The tarsal conjunctiva (lining the interior surface of the lids) may become inflamed as a result of a chronic foreign body in the eye, such as a contact lens or an ocular prosthesis.

KERATITIS

Keratitis is an inflammation or infection of the cornea that can be caused by a variety of microorganisms or by other factors. The condition may involve the conjunctiva and/or the cornea. When it involves both, the disorder is termed keratoconjunctivitis.

NURSING MANAGEMENT: INFLAMMATION AND INFECTION IN THE EYE

CORNEAL SCARS AND OPACITIES

The cornea is an optically transparent tissue that allows light rays to enter the eye and focus on the retina, thus producing a visual image. Any wound causes the cornea to become abnormally hydrated and decreases the normal transparency. A bandage contact lens can be effective in correcting the irregular astigmatism that results from corneal scars. In other situations the treatment for corneal scars or opacities is a keratoplasty. The most commonly used corneal transplant procedure, the penetrating keratoplasty, treats the cornea as a single-layered tissue, while the lamellar keratoplasty specifically targets the diseased layers. This focused surgery spares normal anatomy and can improve clinical outcome. Endothelial lamellar transplantation avoids full-thickness wounds, which are responsible for the slow visual recovery and uncontrolled refractive results that often occur with penetrating keratoplasty. Anterior lamellar transplantation does not replace normal host endothelium, thereby avoiding the risks of endothelial rejection, late endothelial failure and the long-term usage of topical steroids.²⁸

Prior to transplanting the donated corneas, donors are tested for human immunodeficiency virus (HIV) and hepatitis B and C. The tissue is preserved in a special nutritive solution and can be stored for up to a month if used for transplantation. Improved methods of tissue procurement and preservation, refined surgical techniques, postoperative topical corticosteroids and careful follow-up have decreased graft rejection rates.

KERATOCONUS

Keratoconus is a non-inflammatory, usually bilateral disease that is familial but has no exclusive inheritance pattern. It can be associated with Down syndrome, atopic dermatitis, Marfan’s syndrome, aniridia (congenital absence of the iris) and retinitis pigmentosa (hereditary disease characterised by bilateral primary degeneration of the retina beginning in childhood and progressing to blindness by middle age), but most cases of keratoconus are sporadic.

The anterior cornea thins and protrudes forwards, taking on a cone shape. Keratoconus usually appears during adolescence and slowly progresses between 20 and 60 years of age. The only symptom is blurred vision caused by the variable astigmatism associated with the altered corneal shape. The astigmatism may be corrected with glasses or rigid contact lenses. The cornea can perforate as central corneal thinning progresses. Penetrating keratoplasty is indicated when management of refractive error is unsatisfactory and before perforation in advanced cases. Current research in Australia is evaluating the use of riboflavin combined with UVA treatment to confirm the efficacy and safety profile for a new treatment for keratoconus.²⁹

AETIOLOGY AND PATHOPHYSIOLOGY

It is now believed that the development of cataracts is a normal part of the ageing process. By about 70 years of age almost everyone will have some degree of cataract formation. Cataracts can, however, be associated with other factors.³¹ These include blunt or penetrating trauma, congenital factors such as maternal rubella, radiation or UV light exposure, certain drugs such as systemic corticosteroids or long-term topical corticosteroids and ocular inflammation. People with diabetes mellitus tend to develop cataracts at a younger age than do people without diabetes.

Cataract development is mediated by a number of factors. In degenerative cataract formation, it appears that altered metabolic processes within the lens cause an accumulation of water and alterations in the lens fibre structure. These changes affect lens transparency, causing vision changes.³¹

CLINICAL MANIFESTATIONS

The patient with cataracts may complain of a decrease in vision, abnormal colour perception and glare. Glare is due to light scatter caused by the lens opacities and may be significantly worse at night when the pupil dilates. The decline of vision is gradual but the rate of cataract development varies from patient to patient. Some patients may complain of a sudden loss of vision because they inadvertently cover their unaffected eye and the decreased acuity of the eye with cataracts becomes suddenly apparent. Secondary glaucoma can also occur if the enlarging lens causes increased intraocular pressure (IOP).

DIAGNOSTIC STUDIES

Diagnosis is based on decreased visual acuity or other complaints of vision changes. The opacity is directly observable by ophthalmoscopic or slit lamp microscopic examination. A totally opaque lens creates the appearance of a white pupil. Box 21-1 outlines other diagnostic studies that may be helpful in evaluating the visual impact of a cataract.

MULTIDISCIPLINARY CARE

The presence of a cataract does not necessarily indicate a need for surgery. For many patients the diagnosis is made long before they actually decide to have surgery. Non-surgical therapy may postpone the need for surgery. Multidisciplinary care for cataracts is presented in Box 21-1.

Surgical therapy

When palliative measures no longer provide an acceptable level of visual function, the patient is an appropriate candidate for surgery. The patient’s occupational needs and lifestyle changes are also factors affecting the decision to have surgery. In some instances, factors other than the patient’s vision needs may influence the need for surgery. Lens-induced problems, such as an increased IOP, may require lens removal. Opacities may prevent the ophthalmologist from obtaining a clear view of the retina in the patient with diabetic retinopathy or other sight-threatening pathology. In those cases the cataract may be removed to allow visualisation of the retina and adequate management of the problem.

Preoperative phase

The patient’s preoperative preparation should include an appropriate history and physical examination. Because almost all patients have local anaesthesia, many doctors and surgical facilities do not require an extensive preoperative physical assessment. However, most cataract patients are older adults who may have several medical problems that should be evaluated and controlled before surgery. Patients may need to discontinue any anticoagulation therapy for a few days preoperatively.

Almost all cataract patients are admitted to a day surgery facility on an outpatient basis. On the day of admission the patient should not have food or fluids for approximately 6–8 hours before surgery. The nurse will instil dilating drops to help maintain pupil dilation. One type of drug used for dilation is a mydriatic (vasoconstrictor), an α-adrenergic agonist (sympathomimetic) that produces pupillary dilation by contraction of the iris dilator muscle. Another type of drug is a cycloplegic, an anticholinergic agent that produces paralysis of ciliary muscles, and hence accommodation (cycloplegia), by blocking the effect of acetylcholine on the ciliary body muscles. Cycloplegics produce pupillary dilation (mydriasis) by blocking the effect of acetylcholine on the iris sphincter muscle. Examples of mydriatics and cycloplegics are listed in Table 21-4. The patient often receives preoperative antianxiety medication before the local anaesthesia injection.

TABLE 21-4 Topical medications for pupil dilation

DRUG THERAPY

Intraoperative phase

Cataract extraction is an intraocular procedure. Phacoemulsification is the most commonly used technique, in which the nucleus is fragmented by ultrasonic vibration and aspirated from inside the capsular bag (see Fig 21-3).³² An artificial IOL is then inserted into the lens capsule. The incision is usually approximately 3 mm, thereby not requiring sutures. Extracapsular extraction is less commonly performed, but is effective for those patients whose cataract is not suitable for phacoemulsification. A small incision is made, the anterior capsule is opened and the lens nucleus and cortex are removed, leaving the remaining capsular bag intact. The artificial IOL is inserted and fixed into position. The incision is then closed with sutures. Rarely, intracapsular extraction is performed in which the entire lens is removed with the capsule intact (this procedure may be necessary in instances of trauma). Almost all patients now have an IOL implanted at the time of cataract extraction surgery. Because most patients have a phacoemulsification procedure, the lens of choice is a posterior chamber lens that is implanted in the capsular bag behind the iris. At the end of the procedure, the patient receives injections of subconjunctival corticosteroid and antibiotic medications.³³ Then an antibiotic and corticosteroid ointment is applied and the patient’s eye is covered with a patch and protective shield. The patch is usually worn overnight and removed during the first postoperative visit.

Figure 21-3 Phacoemulsification of a cataractous lens through a self-sealing, scleral-tunnel incision. Note the circular opening in the anterior lens capsule.

Postoperative phase

Unless complications occur, the patient is usually ready to go home within a few hours after the surgery as soon as the effects of sedative agents have dissipated. Postoperative medications usually include antibiotic and corticosteroid drops to prevent infection and decrease the postoperative inflammatory response. There is some evidence that postoperative activity restrictions and night-time eye shielding are unnecessary. However, many ophthalmologists still prefer that the patient avoid activities that increase the IOP, such as bending or stooping, coughing or lifting. Ophthalmologists may also recommend using an eye shield over the operative eye at night for protection.

The ophthalmologist will usually see the patient two to three times at increasing intervals throughout the 6–8 weeks following surgery. During each postoperative examination the surgeon will measure the patient’s visual acuity, check anterior chamber depth, assess corneal clarity and measure the IOP. A flat anterior chamber may cause adhesions of the iris and cornea. The cornea may become hazy or cloudy from intraoperative trauma to the endothelium. Even on the first postoperative day the patient’s uncorrected visual acuity in the operative eye may be good. However, it is not unusual or indicative of any problem if the patient’s visual acuity is reduced immediately after surgery. The postoperative eye drops are gradually reduced in frequency and finally discontinued when the eye has healed. The newest innovation is a multifocal IOL that corrects for both near and far vision. Regardless of the type of IOL used, however, patients may still need glasses to achieve their best visual acuity.

NURSING MANAGEMENT: CATARACTS

AETIOLOGY AND PATHOPHYSIOLOGY

There are many causes of retinal detachment. The most common cause is a retinal break. Retinal breaks are interruptions in the full thickness of the retinal tissue and they can be classified as tears or holes. Retinal holes are atrophic retinal breaks that occur spontaneously. Retinal tears can occur as the vitreous humour shrinks during ageing and pulls on the retina. The retina tears when the traction force exceeds the strength of the retina. Once there is a break in the retina, liquid vitreous can enter the subretinal space between the sensory layer and the retinal pigment epithelium layer, causing a rhegmatogenous retinal detachment. Less frequently, retinal detachment can occur when abnormal membranes mechanically pull on the retina. These are called tractional detachments. A third type of retinal detachment is the secondary or exudative detachment that occurs with conditions that allow fluid to accumulate in the subretinal space (e.g. choroidal tumours, intraocular inflammation). Risk factors for retinal detachment are listed in Box 21-3.

CLINICAL MANIFESTATIONS

Patients with a detaching retina describe symptoms that include photopsia (light flashes), floaters and a cobweb, hairnet or ring in the field of vision. Once the retina has detached, the patient describes a painless loss of peripheral or central vision, like a curtain coming across the field of vision. The area of visual loss corresponds to the area of detachment. If the detachment is in the superior nasal retina, the visual field loss will be in the inferior temporal area. If the detachment is small or develops slowly in the periphery, the patient may not be aware of a visual problem.

DIAGNOSTIC STUDIES

Visual acuity measurements should be the first diagnostic procedure with any complaint of vision loss (see Box 21-4). The retinal detachment can be directly visualised using direct and indirect ophthalmoscopy or slit lamp microscopy in conjunction with a special lens to view the far periphery of the retina. Ultrasound may be useful to identify a retinal detachment if the retina cannot be directly visualised (e.g. when the cornea, lens or vitreous humour is hazy or opaque).

MULTIDISCIPLINARY CARE

The ophthalmologist will carefully evaluate the patient with retinal breaks to determine whether prophylactic laser photocoagulation or cryopexy is necessary to avoid possible retinal detachment. Some retinal breaks are not likely to progress to detachment and the ophthalmologist will simply watch the patient, giving precise information about the warning signs and symptoms of impending detachment and instructing the patient to seek immediate evaluation if any of those signs or symptoms are recognised. The general ophthalmologist will usually refer the patient with retinal detachments to a retinal specialist. Treatment of retinal detachment has two objectives. The first is to seal any retinal breaks and the second is to relieve inward traction on the retina. Several techniques are used to accomplish these objectives.

Surgical therapy

Laser photocoagulation and cryopexy

These techniques seal retinal breaks by creating an inflammatory reaction that causes a chorioretinal adhesion or scar. Laser photocoagulation involves using an intense, precisely focused light beam, such as the argon laser, to create an inflammatory reaction. The light is directed at the area of the retinal break. This produces a scar that seals the edges of the hole or tear and prevents fluid from collecting in the subretinal space and causing a detachment. The ophthalmologist may use photocoagulation alone if there is a single small tear with no detachment in the periphery and minimal subretinal fluid. For retinal breaks accompanied by significant detachment, the surgeon may use photocoagulation intraoperatively in conjunction with scleral buckling. Tears or holes without accompanying retinal detachment may be treated prophylactically with laser photocoagulation if the ophthalmologist judges them to be at high risk of progressing to retinal detachment.³⁷ When used alone, laser therapy is an outpatient procedure that usually requires only topical anaesthesia, and the patient generally experiences minimal adverse symptoms during or following the procedure.

An alternative method used to seal retinal breaks is cryopexy. This procedure involves using extreme cold to create the inflammatory reaction that produces the sealing scar. The ophthalmologist applies the cryoprobe instrument to the external globe in the area over the tear. This is usually done on an outpatient basis and under local anaesthesia. As with photocoagulation, cryotherapy may be used alone or during scleral buckling surgery. The patient may experience significant discomfort and eye pain following cryopexy. The nurse should encourage the patient to take the prescribed pain medication following the procedure.

Scleral buckling

Scleral buckling is an extraocular surgical procedure that involves indenting the globe so that the pigment epithelium, choroid and sclera move towards the detached retina. This not only helps seal retinal breaks but also helps relieve inward traction on the retina. The surgeon sutures a silicone implant against the sclera, causing the sclera to buckle inwards. The surgeon may place an encircling band over the implant if there are multiple retinal breaks, if the surgeon cannot locate suspected breaks or if there is widespread inward traction on the retina (see Fig 21-4). If present, subretinal fluid may be drained, by inserting a small-gauge needle, to facilitate contact between the retina and the buckled sclera. Scleral buckling is usually accomplished under local anaesthesia and the patient may be discharged on the first postoperative day.

Figure 21-4 Retinal break with detachment: surgical repair by scleral buckling technique.

Intraocular procedures

In addition to the extraocular procedures described, retinal surgeons may use one or more intraocular procedures in treating some retinal detachments. Pneumatic retinopexy is the intravitreal injection of a gas to form a temporary bubble in the vitreous humour, which closes retinal breaks and provides apposition of the separated retinal layers. As the intravitreal bubble is temporary, this technique is combined with laser photocoagulation or cryotherapy. The patient with an intravitreal bubble must position the head so that the bubble is in contact with the retinal break. It may be necessary for the patient to maintain this position as much as possible for up to several weeks.

Pars plana vitrectomy (surgical removal of the vitreous) is performed for rhegmatogenous retinal detachment and to relieve traction on the retina, which may occur in proliferative diabetic retinopathy. The surgery may also include removal of subretinal fluid, photocoagulation to seal the retinal breaks and insertion of an internal tamponade, such as gas, oil or, rarely, silicone oil to replace the vitreous.³⁸ An external implant (e.g. scleral buckle) may also be used. In proliferative vitreoretinopathy (PVR), membranes develop in the vitreous cavity and on the retinal surface, exerting traction, which causes folds in the retina. Vitrectomy may be combined with membrane peeling to relieve traction in such cases.

Postoperative considerations in scleral buckling and intraocular procedures

Reattachment is successful in 90% of retinal detachments. Visual prognosis varies, depending on the extent, length and area of detachment. Postoperatively, the patient may be on bed rest and may require special positioning to maintain proper position of an intravitreal bubble. The head must be positioned so that the gas, air or oil is lying against the hole/detachment. If a macular hole has been repaired, it is especially important that the patient is positioned face down for up to a fortnight after surgery. The patient is allowed a brief period hourly to attend to nutritional and comfort needs. If gases have been used it is important that patients are informed that activities such as flying or anaesthetics can adversely affect the gases, causing further expansion and possible occlusion of the central retinal artery. To minimise the risk of an adverse event, a ‘bracelet’ stating the type of gas may be useful to remind the patient of potential complications and to inform other medical staff of the presence of gas. It is removed by the ophthalmologist when there is no evidence of gas in the vitreous cavity.³⁸ Overnight hospitalisation varies according to the surgeon’s preference. The patient may need multiple topical medications, including antibiotics and anti-inflammatory agents. Atropine drops are commonly prescribed to prevent ciliary spasm. The patient should be advised that the prolonged action of these drops may cause photophobia and blurred vision. Activity recommendations also vary according to the surgeon’s preference, the extent of the detachment and the particular repair procedure.

In most cases retinal detachment is an urgent situation and the patient is confronted suddenly with the need for surgery. The patient needs emotional support, especially during the immediate preoperative period, when preparations for surgery produce additional anxiety. When the patient experiences postoperative pain, the nurse should administer prescribed pain medications and teach the patient to take the medication as necessary after being discharged. The patient may go home within a few hours of surgery or may remain in the hospital for several days, depending on the surgeon and the type of repair. Discharge planning and teaching are important, and the nurse should begin this process as early as possible because the patient may not remain hospitalised for long. Patient and family teaching following eye surgery is discussed in Box 21-2.

The level of activity restriction following retinal detachment surgery varies greatly. The nurse should verify the prescribed level of activity with each patient’s surgeon and help the patient plan for any necessary assistance related to activity restrictions. The nurse should teach the patient the signs and symptoms of retinal detachment because of the risk of retinal detachment in the other eye.

AETIOLOGY AND PATHOPHYSIOLOGY

The pathophysiological mechanism is thought to be abnormal accumulation of waste material in the retinal pigment epithelium. People with an ARMD-affected first-degree relative have a 50% lifetime risk of developing ARMD and vision loss, and tend to develop it earlier. Cigarette smokers have a four-fold risk of developing ARMD. Weaker links have been found with obesity, hypertension, macrovascular disease, raised cholesterol level, cumulative light exposure and cataract surgery.³⁹

CLINICAL MANIFESTATIONS

The hallmark sign of ARMD is the appearance of drusen in the fundus, which are found on ophthalmoscopic evaluation. Drusen appear as yellowish exudates beneath the retinal pigment epithelium and represent localised or diffuse deposits of extracellular debris. The patient may complain of blurred vision, the presence of scotomas (blind spots in the central visual field) or metamorphopsia (distortion of vision).⁴⁰

DIAGNOSTIC STUDIES

In addition to visual acuity measurement, the primary diagnostic procedure is ophthalmoscopy. The examiner looks for drusen and other fundus changes associated with ARMD. The Amsler grid test (see Table 20-5) may help define the involved area and provides a baseline for future comparison. Fundus photography and IV angiography with fluorescein and/or indocyanine green dyes may be helpful in further defining the extent and type of degenerative disease.

MULTIDISCIPLINARY CARE

Laser photocoagulation of the abnormal blood vessels when visual acuity is already compromised extensively has been the therapy of choice until recently. The laser seals leaking blood vessels in the retina and reduces the growth of new blood vessels. Vision often does not improve after treatment and may even deteriorate; however, the Macular Photocoagulation Study Group showed that treated patients lose less vision than untreated patients.⁴⁰ At present this type of therapy is recommended for the treatment of well-demarcated lesions outside the fovea and those lesions that are sufficiently removed from the fovea so that treatment does not extend to the centre of the fovea, as the laser destroys the retinal pigment epithelium and photoreceptor cells where it is applied, leaving a blind spot at the scarred area.⁴⁰

One of the first treatments for wet ARMD was photodynamic therapy (PDT), which used verteporfin intravenously and a non-thermal laser to activate the photosensitive drug molecules.⁴⁰ Verteporfin is a photosensitising drug that becomes active when exposed to the low-level laser light wave. Until the drug is completely excreted by the body, it can be activated by exposure to sunlight or other high-intensity light, such as halogen. Therefore, patients are cautioned to avoid direct exposure to sunlight and other intense forms of light for 5 days after treatment. Patients leave the clinic completely covered because any exposure to skin by sunlight could activate the drug in that area, resulting in a thermal burn. This treatment now tends to be reserved for patients who are unable to have antivascular endothelial factor (anti-VEGF) therapy or who have had a poor result from it.

The loss of normal retinal pigment epithelium function can lead to local tissue hypoxia, which may result in oversecretion of several chemical factors. One of these factors is endothelial growth factor. This chemical, along with others, may cause new vessel growth (neovascularisation), the classic sign of wet ARMD. The anti-VEGF medication given to treat this is administered intravitreally every 4–6 weeks for 3 doses. The VEGF Inhibition Study in Ocular Neovasculisation (VISION) found that the earliest of these drugs, pegaptanib sodium, was at least as effective as PDT in slowing the progression of moderate to severe vision loss.⁴¹ The benefit of this medication over PDT is that it was also shown to be effective in patients with lesions previously untreatable with PDT. At present two other anti-VEGF drugs, bevacizumab and ranibizumab, are being used and early results show that they are effective in improving patients’ visual acuity.⁴²

The role of high-dose vitamin therapy, especially vitamins C and E and beta-carotene, in slowing the progression of vision loss has been investigated in several studies, but there appears to be no definitive evidence as to whether the introduction of these dietary elements is justifiable in terms of preventing illness.³⁹

The permanent loss of central vision associated with ARMD has significant psychosocial implications for nursing care. Nursing management of the patient with uncorrectable visual impairment is discussed on pages 472–474 and is appropriate for the patient with ARMD. It is especially important when caring for patients with ARMD to avoid giving the impression that nothing can be done about the problem. Although it is true that therapy will not recover lost vision, much can be done to augment the remaining vision. Just knowing that the healthcare provider has not abandoned them can give these patients a more positive outlook.

AETIOLOGY AND PATHOPHYSIOLOGY

The aetiology of glaucoma is related in most types of glaucoma to the consequences of an elevated IOP. A proper balance between the rate of aqueous production (referred to as inflow) and the rate of aqueous reabsorption (referred to as outflow) is essential to maintain IOP within normal limits. IOP between 10 and 21 mmHg is considered normal. When the rate of inflow is greater than the rate of outflow, IOP can rise above the normal limits. If IOP remains elevated, permanent visual damage may occur. However, a raised IOP is not the only cause of damage to the optic nerve, given that 30–40% of patients with primary open-angle glaucoma have normal pressures. It is thought that the damage may be caused by ischaemia to the optic nerve.⁴⁴

Primary open-angle glaucoma represents 90% of the cases of primary glaucoma. In primary open-angle glaucoma, the outflow of aqueous humour through the trabecular meshwork is impaired due to changes within this sieve-like structure.⁴⁵ Primary angle-closure glaucoma represents the other 10% of cases of primary glaucoma. As the name implies, the mechanism reducing the outflow of aqueous humour is angle closure. Usually, this is caused by the lens bulging forwards as a result of an age-related process. Angle closure may also occur as a result of pupil dilation in the patient with anatomically narrow angles. Dilation causes peripheral iris bulging with the same outcome of covering the trabecular meshwork and blocking the outflow channels. An acute attack may be precipitated by situations during which the pupil remains in a partially dilated state long enough to cause an acute and significant rise in IOP. This may occur because of drug-induced mydriasis, emotional excitement or darkness. Drug-induced mydriasis may occur not only from topical ophthalmic preparations but also from many systemic medications (both prescription drugs and over-the-counter drugs). The nurse should check drug documentation before administering medications to the patient with angle-closure glaucoma and should instruct the patient not to take any mydriatic-producing medications.

In secondary glaucoma, increased IOP results from other ocular or systemic conditions that may block the outflow channels in some way. Secondary glaucoma may be associated with various inflammatory processes that block the outflow channels. Inflammatory processes may also damage the trabecular meshwork. Trauma, intraocular or periorbital neoplasms, iris neovascularisation (new blood vessel growth) and other ocular or systemic disorders may also be associated with secondary glaucoma.

CLINICAL MANIFESTATIONS

Primary open-angle glaucoma develops slowly and without symptoms. The patient reports no symptoms of pain or pressure and usually does not notice the gradual visual field loss until peripheral vision has been severely compromised. Eventually the patient with untreated glaucoma has ‘tunnel vision’ in which only a small centre field can be seen and all peripheral vision is absent.

Acute angle-closure glaucoma causes definite symptoms, including sudden, excruciating pain in or around the eye. This is often accompanied by nausea and vomiting. Visual symptoms include seeing coloured haloes around lights, blurred vision and ocular redness. The acute rise in IOP may also cause corneal oedema, giving the cornea a frosted appearance.

Manifestations of subacute or chronic angle-closure glaucoma appear more gradually. The patient who has had a previous, unrecognised episode of subacute angle-closure glaucoma may report a history of blurred vision, seeing coloured haloes around lights, ocular redness or eye or brow pain.

DIAGNOSTIC STUDIES

IOP is usually elevated in glaucoma. Normal IOP by applanation tonometry is 10–21 mmHg. In the patient with elevated pressure, the ophthalmologist will usually repeat the measurements over a period of time to verify the elevation. Although in some patients with open-angle glaucoma IOP may not be raised, for most patients it will be between 22 and 32 mmHg. In acute angle-closure glaucoma, IOP may be 50 mmHg or higher.

In open-angle glaucoma, slit lamp microscopy reveals a normal angle. In angle-closure glaucoma, the examiner may note a markedly narrow or flat anterior chamber angle, an oedematous cornea, a fixed and moderately dilated pupil, and ciliary injection. Gonioscopy allows better visualisation of the anterior chamber angle.

Measures of peripheral and central vision provide other diagnostic information. Whereas central acuity may remain 6/6 even in the presence of severe peripheral visual field loss, visual field perimetry may reveal subtle changes in the peripheral retina early in the disease process, long before actual scotomas develop. When visual field defects begin to appear, the initial scotoma is a small, football-shaped defect that gradually progresses to a nasal and superior field defect in chronic open-angle glaucoma. In acute angle-closure glaucoma, central visual acuity will be reduced if the patient has corneal oedema, and the visual fields may be markedly decreased.

As glaucoma progresses, optic disc cupping occurs. This is visible with direct or indirect ophthalmoscopy (see Fig 21-5). The optic disc becomes wider, deeper and paler (light grey or white). Optic disc cupping may be one of the first signs of chronic open-angle glaucoma. Optic disc photographs are useful for comparison over time to demonstrate an increase in the cup-to-disc ratio and progressive blanching.

Figure 21-5 A, In the normal eye, the optic disc is pink with little cupping. B, In the glaucomatous eye, the optic disc is bleached and optic cupping is present. (Note the appearance of the retinal vessels, which travel over the edge of the optic cup and appear to dip into it.)

MULTIDISCIPLINARY CARE

The primary focus of glaucoma therapy is to keep IOP low enough to prevent the patient from developing optic nerve damage. This damage is manifested by increasing visual field loss and progressive optic disc cupping. Specific therapies vary with the type of glaucoma. The diagnostic and multidisciplinary care of glaucoma is summarised in Box 21-5.

NURSING MANAGEMENT: GLAUCOMA

AUDITORY PROBLEMS

Problems with the auditory system may include problems with the peripheral auditory system, as well as problems with hearing and the vestibular system. Conditions such as external otitis, otitis media and otosclerosis, as well as the effects of ageing, can all lead to hearing loss. The vestibular system is closely related to the auditory system and symptoms such as vertigo and dizziness may be difficult to distinguish from symptoms related to hearing loss and tinnitus.

AETIOLOGY

Infections or dermatitis, or both, may cause external otitis (see Fig 21-7). Bacteria or fungi may be the cause. The bacteria most commonly cultured are Pseudomonas aeruginosa followed by Klebsiella, Proteus, Escherichia coli and S. aureus. The most common fungi are Candida albicans and Aspergillus organisms.⁴⁷ Fungi are often the causative agents of external otitis, especially in warm, moist climates. The warm, dark environment of the ear canal provides a good medium for the growth of microorganisms.

Figure 21-7 Acute external otitis.

Source: Royal Victorian Eye & Ear Hospital, Medical Photography Department.

CLINICAL MANIFESTATIONS AND COMPLICATIONS

Pain (otalgia) is one of the first signs of external otitis. Even in mild cases, the patient may experience pain that is disproportionate to the infection. Pain is caused by the swelling of the bony ear canal as a result of the inflammatory process. Pain is especially noted on movement of the auricle or on application of pressure to the tragus (directly in front of the ear). Drainage from the ear may be serosanguineous or purulent. If it is the result of an infection caused by Pseudomonas, the drainage will be green and have a musty smell. Temperature elevations occur when there is extensive involvement of the tissue. The swelling of the ear canal can block hearing and cause dizziness.

NURSING MANAGEMENT: EXTERNAL OTITIS

Diagnosis of external otitis is made by observation with the otoscope light using the largest speculum that the ear will accommodate without causing the patient unnecessary discomfort. The eardrum may be normal if it can be seen. Culture and sensitivity studies of the drainage may be done. It can be a very painful condition, so analgesics may be required to control the pain. After the ear canal is cleansed, a cotton wick impregnated with antibiotic and anti-inflammatory medication is placed in the canal. This will help reduce inflammation and the infection. Cotton wicks should be used with caution in young patients and confused or psychotic patients, who may push them further into the ear. Topical antibiotics include polymyxin B, neomycin and chloramphenicol. Nystatin is used for fungal infections. If the surrounding tissue is involved, systemic antibiotics are prescribed. Warm, moist compresses or heat may be applied. Improvement should occur in 48 hours, but 7–14 days are required for complete resolution.

Careful handling and disposal of material saturated with drainage are important. Otic drops (ear drops) should be administered at room temperature because cold drops can cause dizziness in the patient due to stimulation of the semicircular canals. The tip of the dropper should not touch the ear during administration to prevent contamination of the entire bottle of drops. The ear is positioned so that the drops can run down the canal. This position should be maintained for 2 minutes after ear drop administration to allow dispersion of drops. Multidisciplinary care of external otitis is shown in Box 21-6.

NURSING MANAGEMENT: ACUTE OTITIS MEDIA

AETIOLOGY AND PATHOPHYSIOLOGY

Untreated or repeated attacks of acute otitis media may lead to a chronic condition. Chronic infection of the middle ear is more common in persons who experience episodes of acute otitis media in early childhood. Organisms involved in chronic otitis media include S. aureus, Streptococcus, Proteus mirabilis, P. aeruginosa and E. coli. As the mucous membrane is continuous, both the middle ear and the air cells of the mastoid can be involved in the chronic infectious process.

CLINICAL MANIFESTATIONS

Chronic otitis media is characterised by a purulent, mucoid or serous discharge accompanied by hearing loss and occasionally ear pain, nausea and episodes of dizziness or tinnitus (see Fig 21-10). The patient may complain of hearing loss that may be a result of destruction of the ossicles, a tympanic membrane perforation or the accumulation of fluid in the middle ear space. In severe cases the ear may be pushed away from the head by the swelling of the mastoid area. Occasionally, a facial palsy or an attack of vertigo may alert the patient to this condition. Chronic otitis media is usually painless but, if pain is present, it indicates that fluid has accumulated.

Figure 21-10 Chronic otitis media.

Source: Royal Victorian Eye & Ear Hospital, Medical Photography Department.

COMPLICATIONS

Untreated conditions can result in perforation of the tympanic membrane and the formation of a cholesteatoma (an accumulation of keratinising squamous epithelium in the middle ear). Its enlarging tumour-like behaviour may destroy the adjacent bones, including the ossicles. Unless removed surgically, a cholesteatoma can cause extensive damage to the structures of the middle ear, erode the bony protection of the facial nerve, create a labyrinthine fistula or even invade the dura, threatening the brain. Other complications of a cholesteatoma are facial palsy if it erodes the bony protection of the facial nerve, vertigo from the creation of a labyrinthine fistula and neurological deficits if it invades the dura.

DIAGNOSTIC STUDIES

Otoscopic examination may reveal a marginal or central perforation of the tympanic membrane (see Fig 21-11). Some tympanic membranes may be healed but have an area that is more flaccid and thinner, indicating a previous perforation. Culture and sensitivity tests are necessary to identify the organisms involved so that the appropriate antibiotic therapy can be prescribed. The audiogram may demonstrate no loss in hearing or a loss as great as 50–60 dB if the ossicles have been partially destroyed or disarticulated (separated). Sinus X-rays, magnetic resonance imaging (MRI) or a CT scan of the temporal bone may demonstrate bone destruction, the absence of ossicles or the presence of a mass, most likely a cholesteatoma.

Figure 21-11 Three common tympanic perforations. A, Small central perforation (hearing is usually good). B, Large central perforation around the handle of the malleus (hearing is usually poor). C, Marginal perforation of Shrapnell’s membrane (hearing is usually good). Cholesteatomas commonly occur in patients with a marginal perforation and are always present with attic perforation.

MULTIDISCIPLINARY CARE

The aim of treatment is to clear the middle ear of infection (see Box 21-8). Systemic antibiotic therapy is initiated based on the culture and sensitivity results. In addition, the patient may need to undergo frequent evacuation of drainage and debris in an outpatient setting. Antibiotic ear drops and 2% acetic acid drops are also used to reduce infection. If there is a recurrence, the patient may need to be treated with parenteral antibiotics. In many cases of chronic otitis media, additional antibiotic therapy loses its effectiveness as the number of treatments increases.

MULTIDISCIPLINARY CARE

The hearing loss associated with otosclerosis may be stabilised by the use of sodium fluoride with vitamin D and calcium carbonate. These medications retard bone resorption and encourage the calcification of bony lesions. Amplification of sound by a hearing aid can be effective because the inner ear function is normal.

Stapedectomy is the surgical treatment for otosclerosis and is usually performed under local anaesthesia with sedation. The ear with poorer hearing is repaired first and the other ear may be operated on 6 months to a year later. (Multidisciplinary care of otosclerosis is shown in Box 21-10.) In stapedectomy, an endaural incision is made using the operating microscope for visualisation. Generally, the stapes superstructure is removed and a small hole is made in the footplate with a drill or laser. A prosthesis made of stainless steel, Teflon or other synthetic material completes the ossicular chain. Sound is then conducted with the prosthesis. The tympanum is rolled back into normal position and Gelfoam is placed on the flap. A cottonwool ball is placed in the ear canal and a dressing is used to cover the ear. During surgery the patient will often report an immediate improvement in hearing in the operative ear. As a result of the accumulation of blood and fluid in the middle ear, the hearing level decreases postoperatively, but then returns to near-normal levels. After implantation of a stapes prosthesis, 75–85% of patients experience a significant improvement in hearing.⁴⁹

NURSING MANAGEMENT: OTOSCLEROSIS

Nursing management of the patient undergoing a stapedectomy is similar to that for the patient who has undergone a tympanoplasty. Postoperatively, the patient may experience dizziness, nausea and vomiting as a result of stimulation of the labyrinth intraoperatively. Some patients demonstrate nystagmus on lateral gaze because of disturbance of the perilymph. Care should be taken to decrease sudden movements by the patient that may bring on or exacerbate dizziness. Actions such as coughing, sneezing, lifting, bending and straining during bowel movements should also be minimised.

NURSING AND COLLABORATIVE MANAGEMENT: MÉNIÈRE’S DISEASE

Multidisciplinary care of Ménière’s disease (see Box 21-11) includes diagnostic tests to rule out CNS disease. The audiogram demonstrates a mild low-frequency sensorineural hearing loss in the affected ear. Speech discrimination is often diminished in the affected ear. Vestibular tests are performed to determine whether dizziness is caused by inner ear disturbance. One such test is the caloric test, where the ear is irrigated with warm or cool water or air. This results in nystagmus or rapid eye movements, which assists the doctor in analysing inner ear function. Other tests include measurement of inner ear fluid pressure, an auditory brain stem response (ABR), a computerised test of the hearing nerves and brain pathways and, as these symptoms may be caused by other conditions such as tumours, a CT scan or MRI may be required.

During the acute attack, antihistamines, anticholinergics and benzodiazepines can be used to decrease the abnormal sensation and lessen symptoms such as nausea and vomiting. Acute vertigo is treated symptomatically with bed rest, sedation and antiemetics or drugs for motion sickness administered orally, rectally or intravenously. The patient requires reassurance and counselling that the condition is not life-threatening.

Medical management between attacks may include vasodilation, diuretics and antihistamines. Diazepam or prochlorperazine may be used to reduce the dizziness. There is increasing evidence that dietary changes can reduce the frequency of Ménière’s disease episodes. The aim of these changes is to stabilise the body fluid levels to avoid the secondary fluctuations of fluid within the ear. These modifications include eating regular meals, having an adequate intake of low-salt, low-sugar fluids, and avoiding caffeine-containing foods and fluids, such as chocolate, coffee and tea. Caffeine is a stimulant that can make dizziness worse and tinnitus louder. Limiting alcohol to avoid headaches is suggested, as is avoiding smoking as the nicotine constricts blood vessels, thereby decreasing oxygen levels to the inner ear, making the symptoms worse. Approximately 75–85% of patients experience improvement with medical management and supportive therapy. The remainder of patients may, in time, require surgical intervention.

Frequent and incapacitating attacks, reduced quality of life and threatened unemployment are indications for surgical intervention. There are several surgical procedures that may be undertaken. The least invasive is the intratympanic application of gentamicin (also known as chemical labyrinthotomy), which causes partial ablation of the vestibular end organ. It results in a partial loss of balance function in the treated ear, controlling vertigo and usually preserving hearing. Following an initial period of adjustment to the new level of balance function, this treatment is well tolerated. Decompression of the endolymphatic sac and shunting are performed to reduce the pressure on the cochlear hair cells and to prevent further damage and hearing loss. If relief is not achieved, vestibular nerve resection may be performed.⁵² Recurrence of vertigo attacks following this surgery has been reported in patients followed up over a 10-year period. When involvement is unilateral, surgical ablation of the labyrinth, resulting in loss of the vestibular and hearing cochlear function, is performed. Labyrinthectomy with eighth cranial nerve section has the highest rates for control of vertigo attacks.

Nursing interventions are planned to minimise vertigo and provide for patient safety. During an acute attack the patient is kept in a quiet, darkened room in a comfortable position. The patient needs to be taught to avoid sudden head movements or position changes. Fluorescent or flickering lights or watching television may exacerbate symptoms and should be avoided. An emesis basin should be available because vomiting is common. To minimise the risk of falling, the nurse should keep the side rails up and the bed low in position when the patient is in bed. The patient should be instructed to call for assistance when getting out of bed. Medications and fluids are administered parenterally, and intake and output are monitored. When the attack subsides, the patient should be assisted with ambulation because unsteadiness may remain.

Similar nursing care is provided after surgical ablation of the labyrinth. The patient will have severe tinnitus and vertigo, which decrease during a period of days or weeks as the brain adjusts to the loss of vestibular input and postural stability is regained.

TYPES OF HEARING LOSS

Sensorineural hearing loss

Sensorineural hearing loss is caused by impairment of function of the inner ear or its central connections. Congenital and hereditary factors, noise trauma over a period of time, ageing (presbycusis), Ménière’s disease and ototoxicity can cause sensorineural hearing loss. Systemic diseases, such as tuberculosis, syphilis, Lyme disease, CMV, HIV and Paget’s disease of the bone, can also cause sensorineural deafness. Immune diseases, diabetes mellitus, bacterial meningitis and trauma are additional causes of this type of hearing loss.

The two main problems associated with sensorineural loss are the ability to hear sound but not to understand speech, and the lack of understanding of the problem by others. The ability to hear high-pitched sounds diminishes with a sensorineural hearing loss. Consonants are high-pitched sounds that give intelligibility to speech. Words become difficult to distinguish and sound becomes muffled. An audiogram demonstrates a loss in decibel levels in the 4000 Hz range, which can progress to the 2000 Hz range. A hearing aid may help the patient who has a 30 dB loss or more by reducing the strain of trying to hear but the sounds will still be muffled. Presbycusis, which is degenerative change of the inner ear, is a major cause of sensorineural hearing loss in older adults. It is a progressive problem that results in many psychological and communication issues. The management of inner ear diseases such as Ménière’s disease can prevent further hearing loss. If ototoxic drugs are used, hearing should be monitored frequently during treatment. Causes of hearing loss are shown in Figure 21-12.

Figure 21-12 Causes of hearing loss.

CLINICAL MANIFESTATIONS

Manifestations that indicate hearing loss include asking others to speak up, answering questions inappropriately, not responding when not looking at the speaker, straining to hear, cupping a hand around the ear, showing irritability with others who do not speak up and increasing sensitivity to slight increases in noise level. Often the patient is unaware of minimal hearing loss or may compensate by using these mannerisms. Family and friends who get tired of repeating or talking loudly are often the first to notice hearing loss.

Deafness is often called the ‘unseen handicap’ because it is not until conversation is initiated with a deaf adult that the difficulty in communication is realised. It is important that the health professional be aware of the need for thorough validation of the deaf person’s understanding of health teaching. Descriptive visual aids can be helpful.

Interference in communication and interaction with others can be the source of many problems for the patient and family. Often the patient refuses to admit or may be unaware of impaired hearing. Irritability is common because of the concentration with which the patient must listen to understand speech. The loss of clarity of speech in the patient with sensorineural hearing loss is most frustrating. The patient may hear what is said but not understand it. Withdrawal, suspicion, loss of self-esteem and insecurity are commonly associated with advancing hearing loss.

NURSING AND COLLABORATIVE MANAGEMENT: HEARING LOSS AND DEAFNESS

Health promotion

Environmental noise control

Hearing loss can be caused by acute loud noise (acoustic trauma) or by chronic exposure to loud noise (noise-induced hearing loss). Acoustic trauma causes hearing loss from mechanical destruction of parts of the organ of Corti. Some recovery of function may occur in the first weeks after injury but the remaining loss is permanent. Noise-induced hearing loss is probably caused by high-intensity stimulation of the cochlea, resulting in mechanical damage to the hair cells and supporting cells in the organ of Corti.

Sensorineural hearing loss as a result of increased and prolonged environmental noise, such as amplified sound, is occurring in young adults at an increasing rate. Health teaching regarding avoidance of continued exposure to noise levels greater than 85–95 dB is essential. Table 21-7 describes the range of sounds audible to humans.

TABLE 21-7 Range of sounds audible to the human ear

Source: Adapted from American Academy of Otolaryngology, 2009. Available at www.entnet.org.

In work environments known to have high noise levels (>85 dB), ear protection should be worn. Occupational Health and Safety (OHS) standards require ear protection for workers in environments where the noise levels exceed 85 dB consistently. A variety of protectors are available that are worn over the ears or in the ears to prevent hearing loss. Periodic audiometric screening should be part of the health maintenance policies of industry. This provides baseline data on hearing against which to measure subsequent hearing loss.

Nurses should participate in hearing conservation programs in work environments. A hearing conservation program should include noise exposure analysis, provision for control of noise exposure (hearing protectors), measurements of hearing, and employee–employer notification and education. Often a multidisciplinary team, including an industrial OHS nurse, engineer and audiometric technician, is responsible for such a program.

Ear protection should be worn during target shooting and other recreational pursuits with high noise levels. Young adults should be encouraged to keep amplified music at a reasonable level and limit their exposure time. Hearing loss caused by noise is not reversible.

Immunisations

Childhood and adult immunisations, including measles, mumps and rubella (MMR) immunisation, should be promoted. Various viruses can cause deafness as a result of fetal damage and malformations affecting the ear. The period of greatest risk of birth defects due to rubella infection is during the first trimester. If infection occurs early in the second trimester, the result is often permanent hearing impairment.⁵⁵ Women of childbearing age should be tested for immunity. A rubella antibody titre of 1:8 or greater shows that the individual has immunity to rubella. If the titre is less, immunisation with live vaccine should be given. The woman should avoid pregnancy for at least 3 months after being immunised. Immunisation must be delayed if the woman is pregnant. Women who are susceptible to rubella can be vaccinated safely during the postpartum period.

Ototoxic drugs

The patient’s reaction to drugs that are known to cause ototoxicity should be monitored. Ototoxicity may affect a person’s hearing (auditory or cochlear function) or balance (vestibular function), or both. Ototoxic drugs are capable of damaging one or both branches of the auditory nerve (CN VIII) and the inner ear. Drugs commonly associated with ototoxicity include salicylates, analgesics, antimalarial drugs, loop diuretics, antineoplastic drugs and antibiotics (see Table 21-8). Patients who are receiving these drugs should be assessed for signs and symptoms associated with ototoxicity. The most common symptoms of drug-induced ototoxicity are tinnitus, sensorineural hearing loss and vestibular dysfunction. If these symptoms develop, immediate withdrawal of the drug may prevent further damage and may cause the symptoms to disappear.

TABLE 21-8 Selected drugs reported to cause ototoxicity

IV, intravenous.

Source: From Bryant B, Knights K, Salerno E. Pharmacology for Health Professionals. Sydney: Elsevier; 2003.

Assistive devices and techniques

Hearing aids

It is important that the patient with a suspected hearing loss has a hearing assessment by a qualified audiologist, including examination and audiometric testing. If a hearing aid is indicated, it should be fitted by the audiologist or a speech and hearing specialist. Many types of hearing aids are available, each with advantages and disadvantages: completely-in-the-canal, in-the-canal, in-the-ear, behind-the-ear (see Fig 21-13) and implantable hearing aids. The conventional hearing aid serves as a simple amplifier. For the patient with bilateral hearing impairment, binaural hearing aids provide the best sound lateralisation and speech discrimination. Patients who are motivated and optimistic about using a hearing aid will be more successful users. The nurse must be prepared to give careful instruction on its use and maintenance and to assist the patient during the period of adjustment.

Figure 21-13 Hearing aids are classified into five basic types. A, TRIANO Micro CIC (completely-in-the-canal) hearing aid. B, TRIANO ITC (in-the-canal) hearing aid. C, TRIANO HS (half shell) hearing aid. D, TRIANO ITE (in-the-ear) hearing aid. E, TRIANO 3 BTE (behind-the-ear) hearing aid. The TRIANO product family, its fitting philosophy, and its range of accessories were intended to satisfy individuals of all ages, from infants through senior citizens, who have hearing loss.

Initially, use of the hearing aid should be restricted to quiet situations in the home. The patient must first adjust to voices (including the patient’s own) and household sounds. The patient should also experiment by increasing and decreasing the volume, as situations require. As adjustment to the increase in sounds and background noise occurs, the patient will be ready to try a different listening environment, such as a small party where several people will be talking simultaneously. Then the environment can be expanded to the outdoors. After adapting to controlled situations, the patient will be ready to encounter environments such as a shopping centre or supermarket. Adjustment to different environments occurs gradually, depending on the individual patient.

When the hearing aid is not being worn, it should be placed in a dry, cool area where it will not be inadvertently damaged or lost. The battery should be disconnected or removed. Battery life averages 1 week and patients should be advised to purchase only a month’s supply at a time. Ear moulds should be cleaned weekly or as needed. Toothpicks or pipe cleaners may be used to clear a clogged ear tip.

Speech reading

Speech reading, commonly called lip reading, can be helpful in increasing communication. It allows for approximately 40% understanding of the spoken word. The patient is able to use visual cues associated with speech, such as gestures and facial expressions, to help clarify the spoken message. In speech reading, many words will look alike to the patient (e.g. rabbit and woman). If the patient wears glasses, the glasses should be used to facilitate speech reading. The nurse can help the patient by using and teaching verbal and non-verbal communication techniques, as described in Box 21-12. If a hearing aid is used, it should be readily available to the patient.

BOX 21-12 Communication with the hearing-impaired patient

Non-verbal aids

Draw attention with hand movements.

Have speaker’s face in good light.

Avoid covering mouth or face with hands.

Avoid chewing, eating or smoking while talking.

Maintain eye contact.

Avoid distracting environments.

Avoid careless expression that the patient may misinterpret.

Use touch.

Move close to better ear.

Avoid light behind speaker.

Verbal aids

Speak normally and slowly.

Do not overexaggerate facial expressions.

Do not overenunciate.

Use simple sentences.

Rephrase sentence; use different words.

Write names or difficult words.

Avoid shouting.

Speak in normal voice directly into better ear.

Sign language

Sign language is used as a form of communication for people with profound hearing impairment. It can involve gestures, finger spelling and facial changes such as eyebrow motion and lip/mouth movements. Sign language is not universal. For example, Auslan (Australian Sign Language; see Resources on p 506) is the language of the deaf community in Australia, and New Zealand Sign Language (NZSL; see Resources on p 506) is unique to New Zealand.

Cochlear implant

The cochlear implant is used as a hearing device for the profoundly deaf. The system consists of a surgically implanted induction coil beneath the skin behind the ear and an electrode wire placed in the cochlea (see Fig 21-14). The implanted parts interface with an externally worn speech processor. The system stimulates auditory nerve fibres by means of an electric current so that signals reach the brainstem’s auditory nuclei and ultimately the auditory cortex. The implant is intended for patients whose sensorineural hearing loss is either congenital or acquired and for whom hearing aids are not helpful. The ideal candidate is one who has become deaf after acquiring speech and language. Adults who were born deaf or became deaf before learning to speak or understand language may have difficulty using a cochlear implant. This is because it is thought that some memory of sound is necessary in order to make sense of the signals passed to the brain by the implant. While there is still debate about when is it best to undertake implants, studies have suggested that cochlear implants fitted in children of 2–6 years of age have the best results.⁵⁶

Figure 21-14 Cochlear implant.

The implant offers the profoundly deaf the ability to hear environmental sounds, including speech, at comfortable loudness levels. Multichannel cochlear implants also serve as aids to speech production. Extensive training and rehabilitation are essential to receive maximum benefit from these implants. The positive aspects of a cochlear implant include providing sound to the person who has heard none, improving lip reading, monitoring the loudness of the person’s own speech, improving the sense of security and decreasing feelings of isolation. With continued research the cochlear implant may offer the possibility of aural rehabilitation for a wider range of hearing-impaired individuals.

Assisted listening devices

Numerous devices are now available to assist the hearing-impaired. Direct amplification devices, amplified telephone receivers, alerting systems that flash when activated by sound, an infrared system for amplifying the sound of the television, and a combination FM receiver and hearing aid are all aids that can be explored by the nurse based on patient needs.

Gerontological considerations: hearing loss

Presbycusis, which is hearing loss associated with ageing, includes the loss of peripheral auditory sensitivity, a decline in word recognition ability, and associated psychological and communication issues. Consonants (high-frequency sounds) are the letters by which spoken words are recognised and the ability of the older person with presbycusis to understand the spoken word is greatly affected. Vowels are heard but some consonants fall into the high-frequency range and cannot be differentiated. This may lead to confusion and embarrassment because of the difference between what was said and what was heard.

The cause of presbycusis is related to degenerative changes in the inner ear, such as loss of hair cells, reduction of blood supply, diminution of endolymph production, decreased basilar membrane flexibility and loss of neurons in the cochlear nuclei. Noise exposure is thought to be a common factor related to presbycusis. Table 21-9 describes the classification of specific causes and associated hearing changes of presbycusis. Often, more than one type of presbycusis may be present in the same person. The prognosis for hearing depends on the cause of the loss. Sound amplification with the appropriate device is often helpful in improving the understanding of speech. In other situations an audiological rehabilitation program can be valuable.

TABLE 21-9 Classification of presbycusis

* Abnormally rapid increase in loudness as sound intensity increases.

Older adults are often reluctant to use a hearing aid for sound amplification. Reasons cited most often include cost, appearance, insufficient knowledge about hearing aids, amplification of competing noise and unrealistic expectations. Most hearing aids and batteries are small, and neuromuscular changes, such as stiff fingers, enlarged joints and decreased sensory perception, often make the care and handling of a hearing aid a difficult and frustrating experience for an older person. Some elderly people may also tend to accept their losses as part of getting older and believe there is no need for improvement.

Argon laser trabeculoplasty

CASE STUDY

Patient profile

Anne Richards, a 60-year-old Indigenous Australian woman with rheumatoid arthritis, returns to the clinic in North Queensland for follow-up care of primary open-angle glaucoma. Her current medical regimen includes topical timolol 0.25% twice daily and latanoprost 0.005% 1 drop at night. Her intraocular pressures are stable on this regimen.

Subjective data

• Reports stable vision

• States she is not always successful in getting the eyedrops instilled because her hands are gnarled and painful from rheumatoid arthritis

Multidisciplinary care

• Brimonidine 0.2% one drop twice daily 15 minutes before procedure

• Argon laser trabeculoplasty (ALT) in the right eye

• Postoperatively, check intraocular pressure 1 hour after ALT

• Discharge medication 1% topical corticosteroid three times daily OD

• Continue previous antiglaucoma drug regimen

• Follow-up in 2 weeks for possible ALT in the left eye

Objective data

• Distant and near visual acuity is stable at 6/12 OU

• Goldmann visual field testing reveals a new scotoma in the right eye

CRITICAL THINKING QUESTIONS

1. Explain the aetiology of this patient’s new scotoma.

2. Why might ALT be an appropriate therapy in this case?

3. What is the purpose of the topical corticosteroid drops after the laser procedure?

4. What topics should the nurse discuss with this patient in discharge teaching?

5. What is the therapeutic goal of ALT?

6. Based on the assessment data, write one or more appropriate nursing diagnoses. Are there any collaborative problems?

Nursing research issues

1. What are the main coping strategies of the patient with severe visual impairment? How can the nurse best support these strategies?

2. What strategies are most effective in teaching patients about avoiding sources of ocular irritation?

3. What factors contribute to the decision-making process for a patient with cataracts who chooses surgery over continued palliative therapy?

4. Are there significant differences in outcomes for older patients when postoperative care following eye surgery includes visits by a home healthcare nurse?

5. How does family support significantly influence patient use of and adjustment to a hearing aid?

6. What motivates a patient to comply with the therapeutic regimen following a tympanoplasty?