Chapter 21:
Preventive Ophthalmology
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Preventive medicine is increasingly important in attempts to fulfill society's expectations of modern medicine with the resources available. Although prevention is a logical approach to the solution of many problems in all branches of medicine, in practice there are a number of hurdles to be overcome. For any particular condition, it is essential that individuals at risk be easily identified. If their identification requires population screening, the screening process should be easy to perform, accurate, and reliable. Preventive measures must be both effective and acceptable to the target population. Unwarranted interference with the at-risk individual's lifestyle only leads to poor compliance. Legislation may be required for certain measures but may engender resentment when it is felt to infringe on personal liberty. For preventive medicine to be successful, there must be cooperation among all segments of society-not just the medical community-in identifying problem areas, establishing workable solutions, and disseminating information. The successes that have been achieved in occupational health are an example of what can be accomplished if a consensus of opinion is established.
In ophthalmology, the major avenues for preventive medicine are ocular injuries and infections, genetic and systemic diseases with ocular involvement, and ocular diseases in which the early treatable stages are often unrecognized or ignored.
PREVENTION OF OCULAR INJURIES
Approximately 1 million Americans have visual loss due to trauma, of which 75% are blind in one eye, and approximately 50,000 suffer serious sight-threatening injuries each year. Young men and children are particularly prone to suffer major ocular trauma. Simple measures are available for prevent- ing many injuries to the eye.
Occupational Injuries
Many manufacturing processes pose a particular threat to the eye. Grinding or drilling commonly propels small fragments of metal into the environment at high velocity, and these missiles can easily lodge on the cornea or penetrate the globe through the cornea or sclera. Tools with sharp ends, such as screwdrivers, are also commonly involved in producing penetrating ocular injuries. Welding arcs produce ultraviolet radiation that may cause epithelial keratitis ("arc eye"). Industrial chemicals-particularly those containing high concentrations of alkali or acid-can rapidly produce severe ocular damage that is often bilateral and associated with a poor visual outcome.
Workers must be properly trained in the use of tools, machinery, and chemicals. Safety guards must be fitted to all machinery, and safety goggles must be worn whenever the worker is doing hazardous work or is in the workplace area where such hazards exist. It is surprising how many workers assume that they are no longer at risk of injury when they are not themselves performing hazardous tasks even though they are in the vicinity of work being performed by others.
The growing interest in "do-it-yourself" projects in the home exposes many more individuals to the risks of ocular injury from machinery, tools, and chemicals. Education of the public about these matters is particularly important, since the risks involved may not be obvious to the ordinary householder or hobbyist.
Early recognition and urgent expert ophthalmologic assessment of any injuries sustained is essential. In the case of chemical injuries, immediate copious lavage of the eyes with sterile water, saline if available, or tap water for at least 5 minutes is the most important method of limiting the damage incurred. Neglect of penetrating injuries or corneal foreign bodies markedly increases the potential for long-term morbidity. Obtaining an accurate history is crucial in identifying the possibility of a penetrating injury. This is particularly true when medical help is sought some time after the injury and the patient may not realize the importance of a seemingly minor episode of trauma. Any worker who presents with unexplained visual loss or intraocular inflammation must be carefully questioned about the possibility of recent ocular injuries and the possibility of an occult intraocular foreign body borne in mind.
Chronic exposure to some industrial processes may lead to ocular damage. For example, improperly screened nuclear materials can lead to early and rapid cataract formation in exposed workers.
Nonoccupational Injuries
The marked reduction in the incidence of severe ocular and facial damage associated with car windshield injuries as a result of legislation requiring the wearing of seat belts is a testament to the effectiveness of such legislation. Similar attempts to reduce the incidence of injuries from fireworks by limiting their availability have not yet been as successful.
Various sports are notorious for the high incidence of severe injuries to the eye, eg, blunt injuries such as in racquetball or penetrating injuries such as in ice hockey. The availability of toughened plastic protective glasses-which can be fitted with refractive correction if required-is a major advance in preventing such injuries.
A large number of ocular injuries are suffered in the home. Corks from bottles of champagne or other sparkling wines can produce severe blunt injuries, and explosion of any bottle containing carbonated beverages may lead to penetrating eye injuries from glass fragments. Unless adequately supervised, children using pencils, scissors, or airguns may sustain or cause serious penetrating injuries.
Unfortunately, a significant proportion of serious ocular trauma results from violent assaults, notably those involving firearms. Prevention requires a reduction in the frequency of such incidents.
Acute keratitis from ultraviolet irradiation as seen after exposure to a welding arc may also occur during skiing if protective goggles are not worn. The role of long-term exposure to ultraviolet light in the etiology of cataract and age-related macular degeneration is still debated. Since the cornea and crystalline lens are effective barriers to the transmission of ultraviolet light-becoming even more effective with age in the case of the crystalline lens-it is hardly surprising that the development of age-related macular degeneration in phakic individuals has not been shown to be related to ultraviolet exposure and thus is not preventable by the use of sunglasses. The effect of ultraviolet light on the maculas of the increasing numbers of aphakic and pseudophakic individuals has yet to be fully assessed. Largely on empirical grounds, ultraviolet filters have been incorporated into many of the intraocular lenses implanted. And individuals without such filters in their intraocular lenses or who are aphakic have been encouraged to incorporate ultraviolet filters in their spectacle lenses or wear appropriate sunglasses whenever possible. There is substantial evidence linking ultraviolet exposure to the development of cataract. But since ultraviolet exposure occurs from the time of birth, advocating the regular use of ultraviolet filters in spectacle lenses or sunglasses as a preventive measure is unlikely to be workable or effective. The role of ultraviolet light exposure in the etiology of certain corneal disorders-particularly pterygium-and of basal cell carcinoma and melanoma of the eyelids is much more widely accepted. Education of the public about the dangers of skin cancer following prolonged sun exposure is very important. Ultraviolet-blocking skin creams should not be used around the eyes, and for that reason reliance must be placed on avoiding unnecessary exposure to the sun or the use of sunglasses. In patients with xeroderma pigmentosum, the eyelids and bulbar conjunctiva frequently develop carcinomas and melanomas, and their development can be minimized, if not prevented entirely, by protective lenses.
Solar retinitis (eclipse retinopathy) is a specific type of radiation injury that usually occurs after solar eclipses as a result of direct observation of the sun without an adequate filter. Under normal circumstances, sun-gazing is difficult because of the glare, but cases have been reported in young people who have suffered self-inflicted macular damage by deliberate sun-gazing, perhaps while under the influence of drugs.
The optical system of the eye behaves as a strong magnifying lens, focusing the light onto a small spot on the macula, usually in one eye only, and producing a thermal burn. The resulting edema of the retinal tissue may clear with minimal loss of function, or it may cause significant atrophy of the tissue and produce a defect that is visible ophthalmoscopically as a macular hole. In the latter event, a permanent central scotoma results. Eclipse retinopathy can easily be prevented by the use of adequate filters when observing eclipses, but the surest way to prevent it is to watch the eclipse on television.
Similar to eclipse retinopathy is the iatrogenic retinal damage that may occur from use of the operating microscope and indirect ophthalmoscope (photic retinopathy). The risk of damage from the operating microscope can be reduced by the use of filters to block both ultraviolet light and the blue portion of the visible spectrum, light barriers such as an opaque disk placed on the cornea, or air injected into the anterior chamber.
PREVENTION OF ACQUIRED OCULAR INFECTION
Infections are a major cause of preventable ocular morbidity. Preventive measures are based on maintenance of the integrity of the normal barriers to infection and the avoidance of inoculation with pathogenic organisms. The pathogenicity of various organisms and the size of the inoculum required to establish infection vary enormously according to the state of the eye. A compromised eye is highly susceptible to infection.
The major barrier to exogenous ocular infection is the epithelium of the cornea and conjunctiva. This can be damaged directly by trauma, including surgical trauma and contact lens wear, or by the secondary effects of other abnormalities of the outer eye, such as lid abnormalities or tear deficiency. In all such situations, particular care must be taken to avoid or recognize secondary infection in its earliest stages.
In the presence of a corneal or conjunctival epithelial defect, particularly when there is an associated full-thickness wound of the cornea or sclera-eg, following penetrating trauma or intraocular surgery-it is essential to use prophylactic antibiotic therapy and most importantly to make certain that any drops or ointments are sterile. Accidental epithelial injury should be avoided whenever possible, particularly in compromised eyes, eg, dry eyes, eyes with corneal exposure due to exophthalmos or abnormal eyelid function such as produced by facial nerve paralysis or ectropion, and eyes with reduced corneal sensation. The classic situation is the combination of fifth and seventh nerve dysfunction such as occurs with cerebellopontine angle tumors, producing a dry, anesthetic eye with poor eyelid closure. Any comatose patient is also at risk of corneal exposure, and prophylactic eyelid taping should be undertaken.
Any unnecessary exposure of the eye to pathogenic organisms should be avoided, but it becomes critical in certain situations. During intraocular surgery, the normal barriers to infection are circumvented, and meticulous attention must be paid to avoiding contamination of the eye with organisms. The ocular environment must be assessed preoperatively to identify and treat any sources of pathogenic organisms. These include colonization or infection of the lacrimal sac, the lid margins, the conjunctiva, and the cornea. In emergency situations, it may only be possible to identify such sources and use prophylactic antibiotic therapy to reduce the chances of subsequent infection, whereas for elective surgery more definitive therapy to eradicate or minimize the pathogenic organisms should be possible. There is much debate about the value of preoperative and perioperative prophylactic antibiotics in patients with no identifiable external ocular disease. It is important to recognize that one of the major causes of endophthalmitis after cataract surgery is Staphylococcus epidermidis, which frequently colonizes normal eyelids. Considerations may need to be given to other sites of bacterial colonization or infection such as the bladder, throat, nose, and skin. Sterility must be ensured of the operative field, instruments, intraocular and topical medications, and other fluids introduced into the eye. During the postoperative period, sterile medications must be used and contact with other patients with established ocular infections avoided.
Contact lens wear is strongly associated with suppurative keratitis due to the combination of an abnormal load of pathogenic organisms and probable recurrent minor trauma to the corneal epithelium. The incidence of suppurative keratitis is particularly high with soft lenses, especially with extended wear. It is apparent that many people wearing contact lenses for cosmetic reasons are not aware of the risks involved. Whereas it may be reasonable to face the risks of infection with extended-wear soft lenses in elderly aphakes who are dependent on contact lenses for refractive correction and cannot cope with daily-wear lenses-or in patients with highly compromised eyes that are symptomatic from bullous keratopathy-the arguments in favor of extended-wear soft lenses for refractive correction in patients with low refractive errors are less strong. A number of patients in this latter group start off their contact lens career using extended-wear disposable lenses, which is of course an attractive arrangement because it dispenses with the need for lens cleaning and the associated paraphernalia, but this practice is likely to require an unwelcome sacrifice of safety for convenience. Contact lens wear exposes the eye to an abnormal load of pathogenic organisms, which have been shown to adhere with particular tenacity to soft lenses, unless the user is absolutely meticulous about contact lens hygiene. The development of toxic reactions to preservatives within the contact lens solutions with the necessary dependence on preservative-free solutions increases the chances of suppurative keratitis from organisms capable of surviving in such solutions, eg, Pseudomonas and Acanthamoeba.
All contact lens wearers must be apprised of the relative risk of suppurative keratitis and the need for meticulous contact lens hygiene. They should be advised to keep a pair of spectacles available so that contact lens wear be discontinued immediately whenever an eye becomes uncomfortable or inflamed. If ocular discomfort or inflammation persists, the wearer should seek ophthalmologic advice without delay.
Neonatal conjunctivitis (see Chapter 17) is a good example of exposure to a heavy load of pathogenic organisms with the added inherent susceptibility of the poorly developed immune mechanisms of the neonatal eye. The major organisms that may produce neonatal conjunctivitis are Neisseria gonorrhoeae, chlamydiae, herpes simplex, Staphylococcus aureus, Haemophilus species, and Streptococcus pneumoniae. Exposure to these organisms occurs during passage down the birth canal. It should be possible to prevent neonatal conjunctivitis by treating mothers harboring these organisms prior to delivery, and this has been achieved for the bacteria, including Chlamydia. The alternative approach is the routine ocular prophylaxis of neonates. This started with the silver nitrate prophylaxis of Credé and has been superseded in a number of centers by topical erythromycin in view of the predominance of chlamydial neonatal conjunctivitis.
Shedding of herpes simplex virus by the expectant mother is not necessarily associated with clinically obvious lesions, and shedding may occur in mothers who do not have any history of such lesions. Identification of mothers likely to infect their babies would require routine viral cultures from all women prior to delivery, and even then it would not be possible to identify specifically those actually shedding virus at the time of delivery. In the presence of frank clinical lesions at the time of delivery, elective cesarean section may be advisable.
PREVENTION OF IATROGENIC OCULAR INFECTION
Ophthalmologists have been clearly implicated in the transmission of infectious eye disease. Outbreaks of epidemic keratoconjunctivitis have been traced to contamination in the ophthalmologist's office. The adenovirus is transmitted via the ophthalmologist's hands, a tonometer, or solutions contaminated by droppers accidentally rubbed against the infected conjunctiva or lid margin of a patient. Contaminated ophthalmic solutions have also been the source of infection in bacterial corneal ulcers and endophthalmitis following intraocular surgery. Pseudomonas aeruginosa used to be a common contaminant of ophthalmic solutions, particularly fluorescein. Instillation of contaminated fluorescein solution to delineate corneal epithelial defects (eg, after removal of a corneal foreign body) may result in severe pseudomonal keratitis and, frequently, loss of the eye.
Other infections can be similarly spread, but their occurrence is not generally recognized. The ophthalmologist should be alert to the possibility that if ophthalmic instruments are improperly sterilized (as by cold sterilization), they may be contaminated with hepatitis B virus. Identification of the acquired immune deficiency syndrome (AIDS) virus in tears has suggested a small possibility of transmission by ophthalmologists. To date, no such incident has occurred.
There is good experimental evidence that applanation tonometer tips can be adequately sterilized, particularly with respect to human immunodeficiency virus type 1, herpes simplex virus, and adenovirus, by wiping with 70% isopropyl alcohol swabs and then allowing the instrument to evaporate dry. It is imperative that the tonometer tip be completely dry before use on the next patient or corneal epithelial damage will result. This method of sterilization is more practical than immersion in alcohol, hypochlorite, or hydrogen peroxide and less likely to damage the tonometer tip, though immersion in such disinfectant solutions at the end of each working day and after examination of high-risk patients is probably advisable. In this case, the tonometer tip should be rinsed in tap water and dried before use. Goldmann three-mirror and similar contact lenses used for patient examination are also susceptible to damage from immersion in disinfectants and should be treated in a similar manner to tonometer tips. The Schiotz tonometer needs to be immersed in disinfectant, autoclaved, or exposed to ethylene oxide for effective sterilization. The noncontact tonometer is recommended for reducing the risks of disease transmission, but it may generate an aerosol spray that endangers the individual operating the tonometer.
Ophthalmologists and their staffs must maintain the highest level of personal hygiene at all times and must use standard sterile technique when appropriate, keeping in mind the possibility of contamination of any solution brought into contact with the eye.
Hands play a major role in the transmission of infection. They should be washed or disinfected (eg, with isopropyl alcohol) before and after the examination of every patient, especially if an ocular infection is thought to be present.
PREVENTION OF OCULAR DAMAGE DUE TO CONGENITAL INFECTIONS
Viral disease of the mother with resultant embryopathy may lead to such ocular anomalies in the offspring as retinopathy, infantile glaucoma, cataract, uveal tract coloboma, etc, and prevention may in some cases be possible. Two viruses, rubella and cytomegalovirus, can be extremely damaging to the infant, and one of them-rubella virus-can be prevented by vaccination. Once a common childhood disease, rubella led to lifelong immunity, but vaccination is now indicated for susceptible young women approaching childbearing age. Susceptibility can be determined by assessing the antibody content of the young woman's blood. If a mother contracts rubella during early pregnancy, she should be informed of the likelihood of ocular and other abnormalities in her baby, and the arguments for and against abortion should be presented.
Unfortunately, cytomegalovirus (the other virus causing a high incidence of congenital anomalies) continues to be a serious and unsolved threat. No protective vaccine is currently available, though one is currently under study.
Toxoplasmosis is another important cause of congenital infection, leading to (1) chorioretinitis, which may be apparent at birth or may remain subclinical until reactivation occurs later in life; (2) cerebral or cerebellar calcification; (3) hydrocephalus; and occasionally (4) more severe central nervous system abnormalities. Unless the mother is immunocompromised, fetal infection occurs only if she acquires primary infection during pregnancy. This can be prevented by eating only meat that is well cooked, by washing vegetables and fruits, and by wearing gloves when disposing of cat litter or working in the garden so that contact with viable oocysts and tissue cysts is avoided. It has been shown that if acute maternal infection during pregnancy can be identified-such as with the serial serologic tests that are required by law in France and Austria-appropriate antibiotic treatment in those pregnancies allowed to proceed, with adjustments according to whether fetal infection is also present, reduces the incidence of congenital infection and improves the clinical outcome in fetuses that are infected.
PREVENTION OF GENETIC DISEASES WITH OCULAR INVOLVEMENT
Until recently, the prevention of genetic disorders received little attention. Now, however, there are genetic counseling centers in many medical centers, and the genetic nature of many disorders that affect the eye is recognized and their transmission better understood than formerly. In conference with internists and pediatricians, it is up to the ophthalmologist to recommend genetic counseling for patients contemplating marriage and children. Patients with histories of childhood diabetes, retinitis pigmentosa, consanguineous mating, retinoblastoma, neurofibromatosis, etc, need genetic counseling to prevent disaster for their offspring.
Some clinical conditions, eg, Down's syndrome (trisomy 21), are associated with an abnormal number of chromosomes or with abnormalities of the sex chromosomes. Prenatal diagnosis can now be made by testing amniotic fluid cells obtained by amniocentesis (a safe and practical procedure), and a positive diagnosis gives the patient the option of abortion.
EARLY DETECTION OF TREATABLE OCULAR DISEASE
A number of primary ocular diseases are treatable only during their early stages or are more effectively treated at that time. Detection of such diseases may be possible through the timely recognition of relevant symptoms or may require specific vigilance on the part of medical workers because of the absence of symptoms.
Age-Related Macular Degeneration
Age-related macular degeneration is the leading cause of permanent visual loss in the elderly in industrialized countries, and its incidence is increasing with each decade over age 50. There are two major forms of the disease: (1) atrophic ("dry") degeneration, in which there is progressive degeneration of the outer retina, retinal pigment epithelium, Bruch's membrane, and choriocapillaris; and (2) exudative ("wet") degeneration, in which there is a sudden onset of visual loss due to leakage of serous fluid or blood into the retina followed by new vessel formation under the retinal pigment epithelium (subretinal neovascular membrane).
Laser photocoagulation of subretinal neovascular membranes may delay the onset of central visual loss but only when the membrane is far enough away from the fovea to permit treatment. Elderly patients developing sudden visual loss due to macular disease-particularly paracentral distortion or scotoma, with preservation of central acuity-should undergo urgent ophthalmic assessment, including fluorescein angiography, to determine their suitability for laser treatment. There is no effective treatment for the atrophic form of macular degeneration except for the provision of low vision aids.
Primary Open-Angle Glaucoma
Primary open-angle glaucoma is a major cause of preventable blindness worldwide, particularly among individuals of African racial origin. About two million Americans have the disease, though half are undiagnosed. The prevalence of primary open-angle glaucoma increases from 0.1% for those aged 40-49 to 3% for those over age 70. Symptoms do not usually occur until there is advanced visual field loss. For treatment to be effective, the disease must be detected at a much earlier stage. Specific screening programs are hampered by the high prevalence of raised intraocular pressure in the absence of glaucomatous visual field loss (ocular hypertension), which is ten times more common than primary open-angle glaucoma, the high frequency of normal intraocular pressure on a single reading in untreated open-angle glaucoma, and the complexities of screening for optic disk or visual field abnormalities.
The best means of detecting primary open-angle glaucoma early is performance of tonometry and direct ophthalmoscopy of the optic disk on all adult patients every 3 years, with referral to ophthalmologists of all those with relevant abnormalities. In the case of patients at high risk of developing primary open-angle glaucoma, such as first degree relatives of affected individuals, formal ophthalmic assessment should take place every year.
PREVENTION OF AMBLYOPIA ("LAZY EYE")
Amblyopia can be defined for the purposes of this discussion as diminished visual acuity in one eye in the absence of organic eye disease. Central vision develops from birth to age 6 or 7; if vision has not developed by then, there is little or no chance that it will develop later. In the absence of eye disease, the two main abnormalities that will prevent a child from acquiring binocular vision are strabismus and anisometropia.
Strabismus
Esotropia or exotropia in a young child causes double vision. The child quickly learns to suppress the image in the deviating eye and learns to see normally with one eye. Unfortunately, vision does not develop in the unused eye; unless the good eye is patched, thus forcing the child to use the deviating eye, sight will never develop in that eye. The child will grow up with one perfectly normal eye that is essentially blind, since it has never developed a functional connection with the visual centers of the brain. This is more likely to occur with esotropia than with exotropia.
Anisometropia
Young children are more concerned with the perception of near objects than with those at a distance. If one eye is nearsighted (myopic) and the other farsighted (hyperopic), the child will favor the nearsighted eye. Thus, the farsighted eye will not be used even though it is straight. The result will be the same as in untreated strabismus, ie, monocular blindness due to failure of visual development in an unused eye. The incidence of anisometropia is about 0.75-1%.
Early Diagnosis
The best way to prevent amblyopia is to test the visual acuity of all preschool children. By the time a child reaches school, it is usually too late for occlusion therapy. The parents can perform the test at home with the illiterate "E" chart. This is sometimes known as the "Home Eye Test." Pediatricians and others responsible for the care of small children should test visual acuity no later than age 4.
Photorefraction is said to be useful in screening for anisometropia, ametropia, astigmatism, and strabismus in preschool children. Any child observed to have strabismus after the age of 3 months should be seen by an ophthalmologist.
PREVENTION OF OCULAR DAMAGE DUE TO SYSTEMIC DISEASES
It is important for nonophthalmologic practitioners, particularly internists, general practitioners, and pediatricians, to be aware of the systemic diseases that have an ophthalmic component which may produce asymptomatic ocular damage.
Diabetic retinopathy is the most common cause of blindness developing between ages 20 and 64. Treatment is available to prevent such blindness, but for best effect it must be administered before visual loss has occurred, ie, diabetics must undergo regular fundal examination and be referred whenever treatment is indicated. The major abnormalities that must be recognized are new vessel formation on the optic disk and exudates around the macula. Any diabetic developing visual loss should also be referred for ophthalmic assessment. (The management of diabetic retinopathy is discussed further in Chapters 10 and 15.)
Uveitis associated with juvenile rheumatoid arthritis is generally asymptomatic in its early stages and often remains undetected until severe loss of vision due to glaucoma, cataract, or band keratopathy has already occurred. Regular ophthalmic screening should take place, particularly of girls with a pauciarticular onset of the disease and circulating antinuclear antibody.
Even in the USA, where it should now be all but unknown, occasional cases of xerophthalmia still occur, and in the underdeveloped areas the world over, where nutrition is often poor, it is still common. Vitamin A deficiency disease, in which the eye changes (xerophthalmia and keratomalacia) are the most damaging and often cause blindness (see Chapter 23), is usually the result of a deficient diet associated with poverty. It should be borne in mind, however, that it may also be associated with chronic alcoholism, weight-reducing diets, dietary management of food allergy, or poor absorption from the gastrointestinal tract due to the use of mineral oil or gastrointestinal disease such as chronic diarrhea.
In vitamin A-deficient children, measles may result in severe corneal disease. Because of the eye signs (ie, night blindness, Bitot's spots, or a lackluster corneal epithelium), the ophthalmologist may be the first to recognize vitamin A deficiency. Early recognition and treatment can prevent loss of vision or blindness due to secondary infection and corneal perforation. Treatment of the acute condition may require large intramuscular doses of vitamin A followed by corrective diet and careful analysis of all possible causes.
PREVENTION OF VISUAL LOSS DUE TO DRUGS
All drugs can cause adverse reactions. It is the ophthalmologist's responsibility to prevent visual loss or major ocular disability from drugs used to treat eye diseases.
Ophthalmic drugs should be packaged and labeled so that mistakes are not made by elderly or poorly sighted patients. Atropine and other strong medications may call for color-labeling. On the first visit to a new ophthalmologist, the patient should be asked to bring along any previously prescribed medications in order to avoid duplication and possible overdosage.
Certain ophthalmic drugs have such frequently occurring and damaging side effects that their use requires special monitoring and special warnings to the patient. Atropine and scopolamine, used to dilate the pupil in iridocyclitis, may precipitate acute glaucoma in certain patients with narrow anterior chamber angles. After prolonged use, they can also lead to conjunctivitis and allergic eczema of the eyelids. Many antiglaucoma drugs can produce stenosis of the puncta and shrinkage of the conjunctiva. Topical anesthetics should never be prescribed or made available for long-term use because severe corneal ulceration and scarring may result.
Corticosteroids used locally in drop or ointment forms may depress the local defense mechanisms and precipitate corneal ulceration, often fungal. They may also worsen herpetic keratitis and other corneal infections and on prolonged use may lead to open-angle glaucoma and to posterior subcapsular cataract. Much of the severity of both herpes simplex virus and varicella-zoster virus corneal infections can be blamed on the unwise use of topical corticosteroids. In this situation, short-term improvement has been traded for long-term disaster.
Many drugs used systemically have serious ocular side effects, eg, keratopathy, retrobulbar neuritis, retinopathy, and Stevens-Johnson syndrome (erythema multiforme). For this reason, the ophthalmologist must take a careful history of the patient's use of drugs as part of the initial examination. Of special interest are the keratopathy and retinopathy that may follow the use of chloroquine in discoid lupus erythematosus. It is the function of the consulting ophthalmologist to detect any early ocular changes and to inform the dermatologist of them so that he can substitute another medication.
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10.1036/1535-8860.ch21