CHAPTER 42 OPHTHALMOLOGIC DISORDERS
Practice of Geriatrics
CHAPTER 42 OPHTHALMOLOGIC DISORDERS
Carol R. Kollarits, M.D.
Common Ocular Problems
Side Effects of Ocular Medications
Blindness and Low Vision
Prevention of Visual Loss
Blindness is the disability feared most by elderly Americans. This fear is rational, since 3% of the patients studied in the mobile population of the Framingham Study cohort were found to be legally blind.1 In a study of geriatric patients confined to nursing homes, more than 25% were found to be legally blind.2
This chapter acquaints the physician caring for geriatric patients with his or her responsibilities in the early diagnosis of potentially blinding eye diseases. In addition, it outlines the elements of emergency management of ocular trauma and the management of common ocular complaints of the elderly. Common surgical techniques and medications used by ophthalmologists are described briefly, since geriatric physicians are often called on to diagnose symptoms arising from interactions and side effects of ocular medications or advise patients about the need for certain types of eye surgery.
Figure 42-1 represents a vertical cross-section through a human eye and orbit. The upper lid is elevated by the action of the levator muscle (innervated by the third cranial nerve). The lids are closed by contraction of the subcutaneous orbicularis muscles (seventh cranial nerve) in both the upper and lower lids. The inner surfaces of the lids are lined with conjunctiva. The conjunctiva forms a continuous lining from the inner surfaces of the lids over the sclera up to the limbus (the junction of the sclera with the cornea). The tear film is composed of mucus from conjunctival goblet cells, aqueous tears secreted by the lacrimal gland, and oil from glands opening at the lid margin. The tear film lubricates the movement of the lids over the cornea.
Figure 42-1 Artist’s representation of a cross-section of the eye.
The cornea is the clear “watch glass” covering of the front of the eye. Its composition is similar to that of the white sclera except that its collagen fibers are arranged more regularly. It is covered by five layers of epithelial cells on its anterior surface. Posteriorly, it is lined by a single layer of endothelial cells that actively pump fluid from the corneal stroma, maintaining the clarity of the cornea.
The anterior chamber is filled with aqueous humor produced by the ciliary body behind the clear lens. The lens is attached to the ciliary body by collagen fibers called zonules. The ciliary body contains muscles that, when contracted, cause the lens to increase its anteroposterior diameter, bringing the eye into focus on near objects.
The central portion of the eye is filled with vitreous humor, a matrix of collagen fibrils interspersed through a gel composed of hyaluronic acid. The retina is 10 cell layers thick and extends from the optic nerve to the edge of the ciliary body. The choroid is a vascular layer that underlies the retina. The tough white outer coat of the eye is the sclera. The optic nerve consists of axons from the nerve fiber layer of the retina. These axons form synapses in the lateral geniculate body on second-order neurons whose axons proceed to the occipital cortex.
The six extraocular muscles insert into the sclera to move the eye. The lateral rectus muscle is innervated by the sixth cranial nerve. The superior oblique muscle is innervated by the fourth cranial nerve. The medial rectus, inferior rectus, inferior oblique, and superior rectus, as well as the previously mentioned levator muscle, are innervated by the third cranial nerve. The sphincter muscle of the iris is innervated by parasympathetic fibers carried in the third cranial nerve. The dilator muscle of the pupil is innervated by sympathetic fibers.3
The screening area of every physician’s office should be equipped with a well-illuminated Snellen chart for estimating visual acuity at a distance of 20 feet. The examiner should obtain the best corrected visual acuity of each eye separately using the patient’s current spectacles. Pupil light responses should be checked with a flashlight, including use of the “swinging flashlight test” for every patient (Fig. 42-2). Ophthalmoscopy is accomplished more easily if the patient’s pupils are dilated. One drop of 2.5% phenylephrine hydrochloride (Neosynephrine) in each eye will dilate the pupils of most eyes with blue irises within 15 to 20 minutes, usually without elevating blood pressure. More darkly pigmented eyes require two to three sets of drops, given at 5-minute intervals. The only contraindications to pupillary dilation are recent head injury, a history of angle-closure glaucoma, or previous admonition by an ophthalmologist that the patient’s pupils should not be dilated.
Figure 42-2 Swinging flashlight test for a Marcus Gunn afferent pupillary defect. In dim illumination, the blind left eye has the same size pupil as its normal fellow eye (A). Illumination of the normal eye causes both pupils to constrict equally (direct and consensual pupillary miosis), as shown in B. Swinging the flashlight over to illuminate the blind eye is followed by dilation of the pupil because the pupil of the blind eye dilates consensually in response to loss of illumination of the normal eye (C). (From Mehelas TJ, Kollarits CR: Pupillary clues to neuro-ophthalmic diagnosis. Postgrad Med 71:199, 1982
COMMON OCULAR PROBLEMS
The most common ocular complaint of Americans over 40 years old is a diminished ability to focus clearly at normal (less than arm’s length) reading distances. This is presbyopia. It is caused by thickening (increased anteroposterior diameter) of the lens within the eye as a result of continued growth of the lens fibers. In the young eye, focusing on a near object is accomplished by contracting the muscles in the ciliary body, which reduces the tension of the zonules and elastic capsule of the lens. The resulting increase in thickness of the anteroposterior lens is allowed to continue until the desired focal distance is reached. In the older eye, the already thickened lens responds more slowly to changes in tension of the elastic capsule. Some individuals notice that they can, with some effort, focus clearly for reading but then when they look up, their distance vision is blurred for several seconds to a few minutes as the lens very slowly resumes its previous anteroposterior diameter. These symptoms are relieved by the use of reading glasses or the addition of bifocal segments to the patient’s distance spectacle correction.
After being presbyopic for many years, some individuals find that they can once again focus clearly for reading without using their bifocals. This “second sight” phenomenon is caused by acquired myopia (nearsightedness) secondary to increasing lens thickness. The protein composition of the lens may change at this time, causing lens opacities (cataract formation).
If the patient experiences pain following an injury, a drop of topical anesthetic can be carefully instilled by gently pulling down the lower eyelid and placing the drop on the conjunctival surface of the lid. The examiner’s fingers should be placed well below the lash margin, and the lid should be pulled away from the eye by rolling the skin over the inferior orbital rim rather than pushing the lid downward. Pushing the lid may transmit pressure to the injured eye, causing pain and prolapse of the vitreous and retina through a corneoscleral laceration. Once the anesthetic drop has been instilled, patients with superficial injuries feel nearly complete relief from pain. Deeper injuries are usually still painful despite the topical anesthetic.
If a corneal abrasion is suspected, it can often be more readily identified by placing a fluorescein strip in the tear film just long enough to color the tears yellow. After the patient blinks, the abraded area of the cornea will stain bright yellow, making it more readily distinguishable from the normal nonstaining corneal surface. Corneal abrasions can be treated by instilling an antibiotic ointment and applying a patch firmly. The lids should be patched tightly enough so that they cannot open under the patch and allow the patch to further abrade the cornea. Use of a patch for 24 hours will permit most corneal abrasions to heal.
If a penetrating ocular injury is suspected on the basis of an irregular pupil, or if an obvious laceration is evident on inspection, the eye should not be patched; rather, a metal shield should be taped over the eye to prevent further damage while the patient is transported to an ophthalmologist for definitive surgical management.
Sudden Visual Loss
In patients who report a sudden loss of vision, visual acuity should be checked with the Snellen chart and recorded. Pupil responses should be examined carefully. In a patient with monocular visual loss resulting from a retinal or optic nerve problem, a Marcus Gunn afferent pupillary defect will be present in that eye when the swinging flashlight test is performed (see Fig. 42-2). If the Marcus Gunn pupil is not present in the affected eye, visual loss is due to an opacity of the media (cataract or vitreous hemorrhage), or there is no visual loss (the patient is hysterical or malingering). If the pupils are normal, confrontation visual field testing should be performed to rule out a homonymous hemianopia due to a stroke, because many patients interpret the loss of the right half of the visual field of each eye as blindness of the right eye.
The most common causes of sudden monocular painless visual loss in the elderly are (1) subretinal hemorrhage (macular degeneration), (2) central retinal artery or vein occlusion, (3) ischemic optic neuropathy (caused by atherosclerosis or giant cell arteritis), (4) retinal detachment, and (5) vitreous hemorrhage resulting from diabetic retinopathy or retinal hole formation. Central retinal artery occlusion can seldom be reversed in time to allow recovery of vision, but the patient requires a work-up for sources of emboli such as atheromatous plaques at the carotid bifurcation or a diseased mitral valve.4 Patients with central retinal vein occlusion also have a poor prognosis for visual recovery. Patients with a branch retinal vein occlusion have a much better chance of recovery of useful vision, but some will require laser treatment. Patients with venous occlusive disease must be evaluated for systemic hypertension, chronic simple glaucoma, and any disease that increases blood viscosity. These include polycythemia, leukemia, the coagulopathies, and macroglobulinemia.
Patients with sudden visual loss in one eye should be examined by an ophthalmologist on an emergency basis. Binocular sudden visual loss is most commonly caused by bilateral occipital lobe infarcts. The pupil responses are normal if the visual loss is a result of occipital infarction.
Gradual Visual Loss
Progressive, unrelenting visual blurring occurring over months or years is most often due to cataracts. Visual loss due to macular degeneration often has an intermittent downhill course. Untreated chronic simple glaucoma results in progressive peripheral visual field loss that the patient may not notice until the central vision is threatened. Gradual visual loss may also be caused by optic nerve atrophy.
Every patient with optic atrophy (pallor of the optic disk) and gradual visual loss should be evaluated for tertiary syphilis, diabetes mellitus, pernicious anemia and other anemias, brain tumor, and poor nutrition (possibly associated with chronic alcoholism and cigarette smoking — “tobacco-ethanol amblyopia”).
Patients with ischemic optic neuropathy may present with optic atrophy in one eye and an apparently edematous disk in the other eye. This is the classic Foster Kennedy syndrome, often ascribed to sphenoid ridge meningioma. However, the most common cause is not meningioma but atherosclerosis or giant cell arteritis. Work-up of the patient with ischemic optic neuropathy should include skull films, determination of erythrocyte sedimentation rate (ESR), and temporal artery biopsy. If the ESR is normal and the skull films are interpreted as normal, a computed tomographic scan of the brain should be obtained to rule out an intracranial tumor. Acute visual loss, whether due to atherosclerosis or giant cell arteritis, should be treated with 100 mg of prednisone by mouth daily for 3 to 5 days. If a diagnosis of giant cell arteritis is made, oral corticosteroids should be continued until the ESR is reduced to normal even if vision is not improved, since patients with this disorder have an increased mortality rate from myocardial infarction if the problem is left untreated. In desperate situations, when steroid therapy has failed to restore vision in the patient’s only remaining eye, transient blood pressure elevation with intravenous levo-norepinephrine may be considered.5
Hereditary causes of progressive optic nerve or retinal degeneration usually become apparent prior to age 50 and will have been diagnosed previously. In the absence of observed ocular abnormalities, unexplained visual loss should be considered the result of a brain tumor until proved otherwise by appropriate studies.
Tearing and Irritation
Many older people are troubled by irritation, the sensation of a foreign body in the eye, or excessive tearing. All these can be symptoms of a “dry eye syndrome.” If no foreign body or trichiasis (misdirected lashes rubbing on the cornea) is found after inspection of the eye with fluorescein staining of the tear film, a presumptive diagnosis of dry eye syndrome can be made. Treatment consists of an artificial tear preparation containing a long-chain polymer that mimics the action of the mucus that is often deficient in the tears of the elderly. Tears II, HypoTears, or a similar preparation should be used at least four times daily and especially before reading or other activities that require frequent eye movements. If the artificial tear preparation does not relieve the excessive tearing, an ophthalmologist should evaluate the patient for dysfunction of the nasolacrimal duct or abnormal lid position.
Irritation may be caused by malposition of the lower lid. Entropion (turning in) and ectropion (turning out) are both caused by laxity of the orbicularis muscle and require surgical procedures that tighten this muscle. Laxity of the orbicularis muscle over the upper lid results in blepharochalasis, the development of an extra lid fold, which often contains herniated orbital fat. This lid fold may hang down on the upper lashes, making it difficult for the patient to elevate the lids sufficiently to see. In true ptosis of the upper lid, the entire lid droops downward over the cornea, and the lid fold disappears. This is usually caused by dehiscence of the levator muscle, but myasthenia gravis and Horner’s syndrome should be ruled out.
Horner’s syndrome may cause minor ptosis of both upper and lower lids, making the affected eye appear smaller because of the narrowed lid fissure. The pupil is smaller in the affected eye than in the other eye, and the skin on the same side of the face produces less sweat. If the patient has no other neurologic signs, a chest film with apical lordotic views should be obtained to rule out the presence of a Pancoast tumor or tuberculosis of the apex of the lung, which affects the sympathetic pathway to the pupil. If the radiographic results are negative and the patient develops no other neurologic symptoms, no further work-up is necessary.
Light Flashes, Floaters, and Visual Hallucinations
Flashing lights that the patient can localize to one eye (rather than half of the visual field in both eyes) are usually due to a vitreous detachment. When the vitreous detaches from the optic nerve, a circular condensation of collagen fibers may float free just in front of the macula and will be seen as a nearly transparent “doughnut” by the patient. Other floaters may be described as “wiggly lines,” “worms,” or “fishnets” that move when the eye moves and continue to move across the patient’s visual field for a short time after the eye stops moving. These floaters are usually no cause for alarm, but floaters appearing as a “swarm of gnats” in the field of one eye usually represent red blood cells from a retinal tear. Since retinal tears may result from vitreous detachment and can cause retinal detachment, a patient with this complaint should be examined by an ophthalmologist. Most elderly patients experience the symptoms of a vitreous detachment, but only 1 in 10,000 develop a retinal detachment.
Brain tumor or cortical ischemia may cause visual hallucinations. When a lesion affects the temporal lobe, the patient may have the sensation that he or she is seeing a movie of some past episode in his or her life. A lesion of the occipital cortex causes unformed hallucinations, such as flashing lights or zigzag lines. The most common example is the visual aura of migraine, which is not necessarily accompanied or followed by a migraine headache. Formed hallucinations, often described as “wallpaper patterns,” sometimes occur in patients who have combined central and peripheral visual loss in both eyes (for example, macular degeneration and glaucoma).
Paralysis of the third, fourth, or sixth cranial nerve may cause diplopia (double vision) that is troublesome to the patient in the field of gaze of the affected extraocular muscle or muscles. Patching the affected eye may be necessary to allow the patient to recover from a cerebral vascular accident or head trauma without the added distraction of diplopia. Corrective muscle surgery is usually not done for 6 months following a head injury or stroke because spontaneous recovery is possible in that time. The young patient who complains of diplopia with one eye covered is usually hysterical, but the elderly individual who describes monocular diplopia often is suffering from a (double focus) cataract. Visual acuity may be quite good with such a cataract, but the diplopia may be sufficiently annoying to justify cataract removal.
Intermittent vertical diplopia is a common sign of basivertebral artery insufficiency in the elderly. Double vision or ptosis that occurs only in the evening is most likely due to myasthenia gravis. If symptoms are not present during a morning examination, another examination should be carried out as late in the day as possible. If double vision or ptosis can be documented at this time, an edrophonium chloride (Tensilon) test may alleviate the symptoms and confirm the suspected diagnosis of myasthenia gravis.
Purulent Discharge and Lid Crusting
Bacterial conjunctivitis is characterized by a purulent discharge that often mats the lids shut when the patient wakes up in the morning. This disorder is not accompanied by pain and should be relieved within 3 to 4 days by frequent use of antibiotic drops.
Infection of the lid margins (marginal blepharitis) is manifest by greasy crusts around the bases of the lashes and swelling and redness of the underlying skin. Warm, moist compresses should be applied to the affected lids four times daily, followed by gentle scrubbing of the lid margins with lid scrub pads or cotton-tipped applicators dipped in baby shampoo. After the lids have been gently dried, a drop of antibiotic solution such as Neosporin should be applied to the inferior cul-de-sac. The common sty (hordeolum) can be treated similarly.
Painless watery discharge, accompanied by conjunctival hyperemia and symptoms of fullness of the lids, is most likely due to a viral or chlamydial conjunctivitis. Topical antibiotics should be used in the same way as for treatment of bacterial conjunctivitis to prevent a bacterial superinfection in these conditions. Sulfonamide eye drops may be used in patients with suspected viral or chlamydial conjunctivitis, but they are not effective in the average case of bacterial conjunctivitis because of the large amount of para-aminobenzoic acid present in purulent discharge.6 If the symptoms last more than 1 week or if the patient complains of pain, an ophthalmologist should be consulted.
Redness, watery discharge, and itching are most commonly caused by allergy. A decongestant-antihistamine preparation (such as Albalon-A or Naphcon-A) should be applied, one drop four times daily. Topical steroid drops should not be used by a physician other than an ophthalmologist because of the danger of potentiating a viral infection and inducing glaucoma. Alomide or Crolom drops prevent histamine release from mast cells in the conjunctiva and are useful for chronic allergic conjunctivitis.
Subconjunctival hemorrhage presents as a dramatic bright red infiltration over the sclera. No treatment other than reassurance should be given, and no work-up is required if the patient has no cutaneous petechial hemorrhages and no history of recent easy bruising or bleeding suggesting a platelet deficiency.
Painful Red Eye
A patient with a red painful eye that has an apparent corneal ulcer (white spot on the cornea) should be referred to an ophthalmologist as an emergency. No antibiotic drops or ointment should be instilled prior to referral, since this may suppress growth of organisms cultured from corneal scrapings. Bacterial corneal ulcers are usually painful, whereas ulcers caused by herpes simplex may not be very painful.
In addition to bacterial or viral corneal ulcers, a red painful eye may be caused by angle-closure glaucoma or iritis. In angle-closure glaucoma the pupil of the affected eye is dilated compared with the pupil of the normal eye, and the eye has a significantly increased intraocular pressure that can easily be detected by finger palpation or tonometry. In iritis, the pupil of the affected eye is smaller than that of the normal eye, and the pressure can be quite low. For either condition, the patient should be referred to an ophthalmologist for definitive management.
At least 2% of the population over the age of 40 have chronic simple glaucoma. In its early stages, this is an asymptomatic disease that, unlike the much rarer acute angle-closure glaucoma, causes no pain. Gradual loss of vision due to prolonged elevation of intraocular pressure is often unnoticed by the patient until a significant amount of the visual field is gone. Patients with optic disk pallor, hemorrhage on the disk, or a progressive increase in the cup-disk ratio over a period of years should be referred to an ophthalmologist for evaluation for possible chronic simple glaucoma. A family history of glaucoma should prompt earlier referral. Glaucoma is the leading cause of irreversible blindness in American blacks. The prevalence of glaucoma in blacks is four to six times higher than that in whites. Other risk factors for glaucoma besides family history and race include diabetes mellitus, cardiovascular disease, and myopia. Patients with these risk factors should have annual examinations by an ophthalmologist.
Most of the medications used to treat glaucoma produce significant side effects. Pilocarpine produces blurring of vision because of induced spasm of accommodation in young patients, and decreased vision because of the decreased pupil size, which in turn reduces the amount of light entering the eye. This may severely reduce vision in an eye with a cataract. Timolol maleate and other beta-blocking drops have been known to precipitate status asthmaticus, congestive heart failure, and psychosis. Epinephrine drops can cause conjunctival redness, browache, and cardiac arrythymias, as well as deposition of pigment in the conjunctiva. The carbonic anhydrase inhibitors acetazolamide (Diamox) and methazolamide (Neptazane) are prescribed to manage severe glaucoma when combinations of eye drops have failed to control the intraocular pressure sufficiently to prevent continued visual loss. Diamox is chemically similar in structure to the sulfonamides and may cause blurred vision, decreased appetite, a metallic taste in the mouth, dizziness, and renal stones. These side effects are less frequent with Neptazane but are not entirely absent. Dorzolamide hydrochloride [Trusopt] is a new topical carbonic anhydrase inhibitor that usually causes no systemic side effects but sometimes causes allergic reactions in patients with a history of allergy to sulfa drugs. Other topical medications for glaucoma include alpha-adrenergic agonists (apraclonidine [Iopidine] and brimonidine tartrate [Alphagan]) and a prostaglandin analogue, latanoprost.7,8 Since the different classes of glaucoma medications lower intraocular pressure by different mechanisms, several of these medications may be combined in a regimen designed specifically for each patient.
The argon laser may be used to treat the trabecular meshwork of eyes in patients with chronic simple glaucoma and progressive visual field loss. If laser trabeculopexy is not successful in lowering intraocular pressure, a surgical trabeculectomy or another fistulizing procedure can be performed.
A recent study of patients with primary openangle glaucoma showed that argon laser trabeculoplasty used as the initial therapy (instead of topical drops) may be more effective in preventing visual field loss. Because 30% of glaucoma patients have significant side effects from eye drops and the current cost of eye drops for glaucoma may be almost $60 for a single month’s supply of one medication, argon laser trabeculoplasty is likely to be performed in a higher percentage of glaucoma patients in the near future.9
Angle-closure glaucoma is much less common than chronic simple glaucoma, but it is less likely to be neglected because its most common symptom is severe pain. The pain results from abrupt elevation of intraocular pressure due to blockage of the trabecular meshwork by the peripheral iris. In addition to pain, the elevated pressure causes corneal edema, creating colored halos around lights observed with the affected eye. The angle closure can be relieved by creating an iridotomy (hole in the iris) with the argon laser or neodynium YAG laser or by surgical iridectomy.
The most common cause of periocular pain is sinus disease. Because of the proximity of the sinuses to the orbit (see Fig. 42-1) and common innervation of these structures by the fifth cranial nerve, sinus pain is often referred to the eye. In the absence of decreased vision, elevated intraocular pressure, or redness, most complaints of ocular pain deserve a trial of oral decongestant therapy.
The lancinating pain of tic douloureux and the throbbing pain of migraine may also involve the eye. Tic douloureux responds well to carbamazepine (Tegretol), whereas migraine may be reduced in frequency by the use of propranolol hydrochloride (Inderal). For patients with frequent debilitating migraine, Inderal 40 mg/day should be tried. This dose may have to be reduced if it produces orthostatic hypotension. Some patients who experience a definite warning aura 15 to 30 minutes prior to the onset of the headache can abort the headache by taking one 10-mg tablet of Inderal and one 5-grain tablet of aspirin as soon as they notice the warning migraine aura. Oral or intramuscular sumatriptan (Imitrex) may be used in patients who do not respond to Inderal.
Pain in the distribution of the ophthalmic division of the trigeminal nerve may be caused by herpes zoster. Often pain may be noted when combing the hair up to 10 days before the appearance of the vesicles. No specific ocular therapy is indicated unless vesicles develop on the tip of the nose on the same side as the “shingles.” When this occurs, the eye is usually severely inflamed, often resulting in chronic pain and accelerated cataract formation. As in any elderly person with herpes zoster, systemic evaluation should be done for leukemia, lymphoma, and other diseases affecting the immune system. Postherpetic pain may be severe and may last for a period of several months. Tegretol is often useful in the management of this pain. Oral acyclovir (Zovirax), 800 mg five times daily for 10 days, or famciclovir (Famvir), 500 mg three times daily for 7 days during the acute attack, may reduce the severity and duration of postherpetic pain.
The cause of throbbing pain accompanied by an ipsilateral paralysis of the third cranial nerve (upper lid ptosis, dilated pupil, eye displaced down and laterally) should be considered an intracranial aneurysm until a normal arteriogram has been obtained. Painful ophthalmoplegia caused by the Tolosa-Hunt syndrome may be treated with steroids after aneurysm and diabetes mellitus have been ruled out. Paralysis of the third cranial nerve caused by diabetes mellitus does not involve the pupil and usually is not accompanied by the severe pain seen in patients with aneurysm or Tolosa-Hunt syndrome. If caused by diabetes, the paralysis will disappear spontaneously within 90 days.
Any decrease in transparency or alteration of the optical homogeneity of the lens is called a cataract. Cataract formation begins in everyone over 30 years of age but progresses at varying rates in different individuals. Total opacification of the lens, resulting in a white, “mature,” or “ripe” cataract, actually occurs in very few people.
Compared with a normal lens, a cataractous lens has different water and ionic concentrations and protein constituents. Some of these changes in lens chemistry may result from exposure to ultraviolet light or other unknown toxic environmental influences. Cataract formation is more common in diabetics because of the increased hydration resulting from the presence of excessive sorbitol and fructose in the diabetic lens. Inhibition of the enzyme aldose reductase reduces sorbitol accumulation in the lens and may retard the development of cataracts in diabetics. Unfortunately, use of topical aldose reductase inhibitors and other eye drops have not reversed cataract changes. For most patients with cataracts, surgical extraction is the only alternative to progressive visual loss.
Cataract extraction is the most commonly performed operation in the United States today, with approximately 1 million being performed each year. The risk of visual loss as a result of cataract surgery is less than 5%.
Cataract phacoemulsification (use of ultrasonic fragmentation of the nucleus) with implantation of a synthetic intraocular lens in the remaining capsular bag is the cataract procedure most commonly performed today because it can be performed through a smaller incision than intracapsular or other types of extracapsular surgery. In phacoemulsification, an opening is made in the anterior capsule. The nucleus of the lens is then fragmented ultrasonically and aspirated, care being taken to avoid damage to the corneal endothelium. The softer cortical material can then be aspirated and peeled away from the remaining capsule before the intraocular lens is implanted. The final spectacle lens for the pseudophakic eye is usually prescribed about 6 weeks following cataract surgery. Accurate intraocular lens power calculation allows the pseudophakic eye to see well with a much thinner spectacle lens than would have to be prescribed for the aphakic eye, eliminating the magnification and distortion produced by “old-fashioned” thick cataract glasses.
In many pseudophakic eyes, the posterior capsule behind the intraocular lens implant opacifies because of proliferation of residual cortical lens fibers across the posterior capsule. If this capsular opacification (secondary cataract or secondary membrane formation) interferes with vision, a neodynium YAG laser can be used to create a clear opening in the posterior capsule, restoring vision. This laser treatment can be done with topical anesthetic drops in a few minutes and often results in restoration of good vision within hours.
If the patient has been advised to have cataract surgery but does not believe that vision is compromised sufficiently to justify surgery, near vision should be checked with the patient wearing current bifocals. If the patient can read newsprint with the affected eye, surgery can usually be deferred. Sometimes the patient is eager to have cataract surgery, but the ophthalmologist may recommend that no surgery be done, often because macular degeneration, diabetic retinopathy, or chronic simple glaucoma has reduced the patient’s vision so much that cataract surgery may provide little or no visual improvement. When other intraocular diseases coexist with a cataract, the timing of cataract surgery becomes a matter of careful judgment by the ophthalmologist.