Preventive OpHthalmology

Preventive OpHthalmology
Redota, Tanbonliong

Introduction Vision is a vital factor influencing the quality of life.
Eye care in the practice of medicine is essential. Vision is a vital factor influencing the quality of life- Eye care in the practice of medicine is essential. 2

Outline I. Prevention of Ocular Injuries II. Prevention of Acquired Ocular Infection III. Prevention of Iatrogenic Ocular Infection IV. Prevention of Ocular Damage due to Congenital Infections V. Prevention of Genetic Diseases with Ocular Involvement VI. Early Detection of Treatable Ocular Diseases VII. Prevention of Amblyopia VIII. Prevention of Ocular Damage Due to Systemic Diseases IX. Prevention of Visual Loss due to Drugs X. Present Studies

Introduction According to WHO: 1 person goes blind every 6 seconds.
1 child goes blind every minute. 75% of cases are PREVENTABLE!

Introduction Preventive medicine Success factors:
Identification of at-risk groups Effectivity and acceptability of preventive measures Legislative policies Cooperation among all segments in society

Avenues for preventive medicine
Ocular injuries and infections Genetic and systemic diseases with ocular involvement Ocular disease in which the early treatable stages are often unrecognized or ignored

Prevention of Ocular Injuries
Occupational and Non-occupational Occupational Trauma Chemical Thermal/Radiation Occupational Injuries Majority of these injuries result from small particles or objects striking or abrading the eye. metal slivers, wood chips, dust, and cement chips nails, staples, or slivers of wood or metal Large objects causing blunt force trauma to the eyeball or eye socket. Majority of these injuries result from small particles or objects striking or abrading the eyeinclude metal slivers, wood chips, dust, and cement chips that are ejected by tools, wind blown, or fall from above a worker. Some of these objects, such as nails, staples, or slivers of wood or metal penetrate the eyeball and result in a permanent loss of vision. Large objects may also strike the eye/face, or a worker may run into an object causing blunt force trauma to the eyeball or eye socket. Chemical burns to one or both eyes from splashes of industrial chemicals or cleaning products are common. Thermal burns to the eye occur as well. Among welders, their assistants, and nearby workers, UV radiation burns (welder’s flash) routinely damage workers’ eyes and surrounding tissue.

Chemical Burns Radiation Burns
Chemical burns to one or both eyes from splashes of industrial chemicals or cleaning products are common. Acid vs Alkali Radiation Burns Among welders, their assistants, and nearby workers, UV radiation burns (welder’s flash) routinely damage workers’ eyes and surrounding tissue epithelial keratitis PICTURE OF EPITHELIAL KERATITIS TREATMENT OF EPITHELIAL KERATITIS

Who are at risk? Manufacturing industry Grinding and drilling industry
Factory workers Welders, carpenters, construction workers

PREVENTIVE TIPS: Proper training of workers in the use of tools, machinery, and safety goggles. Early recognition and urgent expert opthalmologic assessment of any injuries is essential E.g chemical injuries- copius lavage of sterile water for 5 minutes

PREVENTIVE TIPS: Education of the public due to widespread availability of machineries, tools and chemicals. Proper labeling and storage

Nonoccupational injuries Windshield injuries Decreased incidence due to seatbelt legislation Decreased incidence of ocular trauma due to fireworks ban

Nonoccupational injuries Sports related injuries such as in baseball, basketball, hockey, etc. Home based ocular injuries Corks from bottles of champagne or other sparkling wine Use of pencils, scissors, or airguns especially children

Nonoccupational injuries Ultraviolet radiation exposure Associated with pterygium, basal cell carcinoma and melanoma of the eyelids Substantial evidence linking ultraviolet exposure with the development of cataract. FIND STUDIES LINKING UV RADIATION AND CATARACT FIND PICTURES OF PTERYGIUM, BASAL CELL CARCINOMA, MELANOMA

Nonoccupational injuries Solar retinitis (Eclipse retinopathy) Specific type of radiation injury that usually occurs after solar eclipses as a result of direct observation of the sun without adequate filter (Vaugh and Ausbury, 2008) Prevented with use of adequate filters, surest way is to watch the eclipse through the television ECLIPSE RETINOPATHY MAGNIFYING LENS ANALOGY Eye can act as the magnifying lens. Direct observation of the sun can focus the light into a small spot in the macula, producing thermal burns. Edema may result and resolve with minimal loss of function, or atrophy of tissue may develop. Central scotoma/ blind spot in the field of vision may result.

Prevention of Acquired Ocular Infection
Preventive measures are based on maintenance of the integrity of the normal barrier to infection. Disruption can be caused by penetrating trauma or intraocular surgery Use of antibiotic prophylaxis, eye drops Recent studies in India: Bacterial and fungal ulcers occurring after corneal abrasion are successfully prevented by antibiotic ointment 3x/day for three days Major barriers to exogenous ocular infection is the epithelium of the cornea and conjunctiva, which are damaged directly by trauma, including surgical trauma and contact lens wear or by secondary defects of other abnormalities such as lid abnormalities or tear deficiency

High risk Corneal injuries and defects Dry eyes Corneal exposure due to exopthalmos Abnormal eyelid function (e.g facial nerve paralysis, ectropion) Cerebellopontine angle tumors Cerebellopontine angle tumors- dysfunction of the fifth and facial nerve producing a dry, anesthetic eye with poor eyelid closure.

Contact lens wear Associated with suppurative keratitis due to abnormal load of organisms and probable recurrent minor trauma to the corneal epithelium Toxic reactions to preservatives within contact lens solutions Prevention tips: meticulous contact lens hygiene; keeping a pair of spectacles PICTURE OF SUPPURATIVE KERATITIS

Giant papillary conjunctivitis
Usually occurs in soft contact lens wearers Condition that produces a chronic irritative stimulus Typical history: wearing of contact lens and through the years, they become intolerant to the pain

Neonatal conjunctivitis Etiologic agent: Neisseria gonorrhea, chlamydia, Herpes simplex, Staphylococcus aureus, Haemophilus, Streptococcus pneumoniae. Exposure: passage to the birth canal Prevention prongs : Prior treatment of the mother before delivery; ocular prophylaxis of neonates (silver nitrate erythromycin) Picture of opthalmia neonatorum Usually associated with urethritis, cervicitis o Prominent follicular response, non--‐tender preauricular lymphadenopathy  It presents papilla and follicles on the upper tarsal conjunctiva, similar to adenoviral infection. o Punctate Epithelial Chlamydial (Inclusion) keratoconjunctivitis can present like viral conjunctivitis. The difference lies presence of flipping eyelids in inclusion keratoconjunctivitis its absence

Prevention of Iatrogenic Ocular Infection
Epidemic keratoconjunctivitis Traced to the contamination of opthalmologist’s office Organisms transmitted via the opthalmologist’s hand, tonometer, or solutions contaminated by droppers E.g. Pseudomonas aeruginosa contamination of fluorescein Preventive: applanation tonometer tips can be adequately sterilized by wiping with 70% isopropyl alcohol swabs and then allowing the instrument to dry by evaporation Maintenance of the highest level of personal hygiene

Prevention of Ocular Damage Due to Congenital Infections
Retinopathy, infantile glaucoma, cataract, uveal tract coloboma, etc CMV - one vaccine is currently under study. Congenital coloboma (absence of tissue) of iris, ciliary body and choroid

Rubella Rubella vaccine – lifelong immunity indicated for susceptible young women approaching childbearing age Susceptibility can be determined by assessing the antibody titers Rubella during early pregnancy - informed of the likelihood of ocular and other abnormalities in her baby, and the arguments for and against abortion Cytomegalovirus no protective vaccine congenital rubella syndrome: heart deformities hearing loss mental retardation eye deformities prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called "blueberry muffin lesions." [8] For these reasons, Rubella is included on the TORCH complex of perinatal infections. Similar to age-related macular degeneration first dose is given at 12 to 18 months of age with a second dose at 36 months If a pregnant woman is diagnosed with the CMV infection, there are a few ways that the fetus can be checked for infection. Amniocentesis can be done to check fetal fluids or blood for signs of infection. Symptoms that could signify possible infection include low amniotic fluid levels, intrauterine growth restriction, and enlarged tissues in the brain. Once the baby is born, testing can be done by saliva, urine, or blood. What is the treatment for CMV? Maternal CMV infections may be treated with one of two drugs that are used in severe situations of CMV infection. There are no treatments for prenatal or postnatal therapy of the infection. Vaccines for treatment are still in the research and developmental stages. Pregnant women who are healthy are not at special risk for disease from CMV infection. In fact, the incidence of primary maternal CMV infection in pregnant women in the United States varies from 0.7% to 4%. Pregnant women who are infected with CMV rarely have symptoms, but rather their developing baby may be at risk for congenital (meaning from birth) CMV disease. CMV is the most common cause of congenital viral infection in the United States. The transmission rate to the fetus is between 24-75% according to the Organization of Teratology Information Service (OTIS), with an average transmission rate of 40%. Of the 40% of babies who become infected, only 10% show signs of congenital CMV after primary maternal infection. For women who have been infected at least 6 months prior to conception, the rate of newborn CMV infection is about 1%, and these infants appear to have no significant illness or abnormalities. The following potential problems can occur for infants who are infected from their mothers before (during pregnancy) birth: Moderate enlargement of the liver and spleen 80-90% suffer from complications within the first few years of life including hearing loss, vision impairment, and varying degrees of mental retardation. 5-10% will present with no symptoms at birth but will develop varying degrees of hearing and mental or coordination problems. When CMV is transmitted at the time of delivery from contact with genital secretions or later in infancy through breast milk, these infections usually result in few, if any, symptoms or complications.

Cytomegalovirus Throughout your pregnancy practice good personal hygiene, including hand washing with soap and water If you develop a mononucleosis-like illness, you should be checked for CMV infection Refrain from sharing food, eating utensils and drinking utensils with anyone. Test the CMV antibodies to determine if you have already had CMV infection. Breastfeeding benefits outweigh the minimal risk of transmitting CMV Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice). Though severe cases can be fatal, with supportive treatment most infants with CMV disease will survive. However, from 80% to 90% will have complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of mental retardation. Another 5% to 10% of infants who are infected but without symptoms at birth will subsequently have varying degrees of hearing and mental or coordination problems.

Toxoplasmosis chorioretinitis, which may be apparent at birth or may remain subclinical until reactivation occurs later in life; cerebral or cerebellar calcification; hydrocephalus; more severe CNS abnormalities. Causes: mother is immunocompromised

Toxoplasmosis Chorioretinitis
Toxoplasma gondii is an intracellular coccidian parasite and is one of the most common parasitic diseases of animals and man. The definitive hosts for the parasite (the only animals in which the organism reproduces sexually) are members of the Felidae family (mainly domestic cats). T gondii is of primary importance since the range of intermediate hosts which can become infected encompasses virtually all warm-blooded animals, including man. Although infection with T gondii is extremely common, it is rarely a cause of significant disease in any species.

Toxoplasmosis Prevention: By eating only well-cooked meat By washing vegetables and fruits By wearing gloves when disposing of cat litter or working in the garden so as to prevent contact with viable oocysts and tissue cysts Serial serologic tests - required by law in France and Austria

Prevention of Genetic Diseases with Ocular Involvement
Genetic counseling centers Patients with histories of childhood diabetes, retinitis pigmentosa, consanguineous mating, retinoblastoma, neurofibromatosis, etc Down's syndrome (Trisomy 21) - testing amniotic fluid cells from amniocentesis

Age-Related Macular Degeneration
Leading cause of permanent visual loss in the elderly in industrialized countries Incidence increased with each decade over age 50

2 major forms: Atrophic ("dry") Degeneration progressive degeneration of the outer retina, retinal pigment epithelium, Bruch's membrane, and choriocapillaris No treatment Low vision aids Exudative ("wet") Degeneration 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).

Prevention: Laser photocoagulation of subretinal neovascular membranes and photodynamic therapy following IV verteporfin delay the onset of central visual loss but only when the membrane is far enough away from the fovea to permit treatment Translocation of the macula radical surgical approach may benefit a few patients Intravitreal Vascular Endothelial Growth Factor Inhibitors most promising Ex. Ranibizumab (Lucentis) and Bevacizumab (Avastin) Both must be given by repeated intravitreal injection Have regular eye exams. Eye exams may help determine whether you are at risk for developing AMD or, if you have AMD, may detect it early. If it is treatable, early detection may help reduce or delay any loss of vision. Do not smoke. People who smoke may be twice as likely to develop AMD than those who do not smoke.2 Even after you stop smoking, this increased risk may persist for many years. Eat plenty of fruits and nuts. Eating regular servings of fruits and nuts may lower your chances of getting AMD.5 You may help prevent wet AMD if you already have the dry form: Eat a diet rich in dark green, leafy vegetables (such as spinach). Your doctor may also advise you to take antioxidant vitamins and zinc. A diet rich in vitamins may slow the progression of AMD and delay vision loss. But this treatment is most effective if you already have moderate AMD. Check with your doctor before taking any supplements. Some can have harmful side effects, especially in high doses.2 Eat fish. Eating fish, a good source of omega-3 fatty acids, may lower your chances of getting AMD.2 Limit harmful fats. Too much saturated fat and cholesterol in your diet may increase your risk that AMD will get worse.2 Get regular exercise and stay at a healthy weight. These choices may lower your risk of developing wet AMD.

Elderly patients developing sudden visual loss, paracentral distortion or scotoma, with preservation of central acuity urgent ophthalmic assessment Fluorescein Angiography to determine their suitability for treatment

Primary Open-Angle Glaucoma
Major cause of preventable blindness worldwide African or Caribbean race About 2 million Americans have the disease Half are undiagnosed Prevalence increases from 0.1% for those aged 3% for those >70 Symptoms do not usually occur until there is advanced visual field loss Primary open-angle glaucoma is when optic nerve damage results in a progressive loss of the visual field.[55] This is associated with increased pressure in the eye. Not all people with primary open-angle glaucoma have eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown to stop progression even in these cases. The increased pressure is caused by Trabecular blockage which is where the aqueous humor in the eye drains out. Because the microscopic passage ways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is affected first but eventually the entire vision will be lost if not treated. Diagnosis is made by looking for cupping of the optic nerve. Prostaglandin agonists work by opening uveoscleral passageways. Beta blockers such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing formation of Aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine,apraclonidine) both decrease fluid production (via. inhibition of AC) and increase drainage.

Prevention: Early detection Specific Screening Programs Ocular Hypertension 10 times more common than primary open-angle glaucoma high frequency of normal intraocular pressure on a single reading in untreated open-angle glaucoma complexities of screening for optic disk or visual field abnormalities. Tonometry and Direct Ophthalmoscopy of the Optic Disk on all adult patients q3 years Best screening relevant abnormalities first-degree relatives of affected individuals – q1 year. Ocular HTN - increased intraocular pressure in the absence of glaucomatous visual field loss Prevention of chronic glaucoma includes: Regular eye examinations: Every 2 years for those between the age of 40 and 65 Every year for those over 65 Statin medications: Used to lower cholesterol

Amblyopia ("Lazy Eye") 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. 2 main abnormalities: Strabismus Anisometropia

Strabismus Esotropia or exotropia - double vision
The child quickly learns to suppress the image in the deviating eye and learns to see normally with one eye Vision does not develop in the unused eye One perfectly normal eye that is essentially blind, since it has never developed a functional connection with the visual centers of the brain More likely to occur with esotropia than with exotropia Good eye should be patched Strabismus – misalignment of the eyes Eso-duling Exo-banlag The American Association for Pediatric Ophthalmology and Strabismus, the American Academy of Pediatrics, and the American Academy of Family Physicians recommend that at a minimum all children be screened for eye health before age 6 months, regularly during each check-up, and again between 3 and 5 years of age by a pediatrician, family practitioner or ophthalmologist. Routine vision screening for young children includes testing for strabismus, usually using the light reflex for infants, and cover testing for preschool-age children. Some health care professionals screen for vision problems with a special camera that takes instant pictures of a child's eyes. Crescents of light reflected off the eyes can indicate strabismus or other eye problems including nearsightedness, farsightedness and cataracts.

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. Monocular blindness Incidence of anisometropia %. Anisometropia – difference in the refractive error of the eyes Screening for anisometropia in preschool children. K D Fern, R E Manny, R Garza College of Optometry, University of Houston, Texas, USA. PURPOSE: A preschool vision screening program was reviewed to evaluate eccentric photoscreening (EP), visual acuity, and stereopsis in identifying anisometropia. METHODS: Patients referred by the screening were examined to assess efficacy of the three screening techniques in a population of preschool children. Testability and comparison of screening results to the classification of anisometropia (> or = 1 D) by retinoscopy obtained during a complete examination were evaluated. RESULTS: Although EP identified 94.5% of the anisometropic children as abnormal, only 27.8% were classified as anisometropic by EP. Of the anisometropic children, 36.1% failed acuity, but only 19.4% failed based on a 2 line or greater interocular acuity difference. Stereopsis correctly identified only 7.3% of anisometropes as abnormal. CONCLUSIONS: The sensitivity of EP in identifying anisometropic children as abnormal was superior to acuity and stereopsis, yet its ability to identify anisometropia specifically was poor. Anisometropia of low magnitude or that masked by the dead zone of the EP system was frequently classified as isometropic. Altering the EP referral criterion and/or taking photographs through adequate power plus lenses may improve the sensitivity for specifically identifying anisometropia. However, caution must be exercised when using EP to examine the prevalence of anisometropia in a population or if used to screen for only amblyogenic refractive errors (i.e., anisometropia), because many anisometropes will be missed, resulting in inaccurate prevalence data and significant underreferrals.

Amblyopia - Early Diagnosis
Visual Acuity Test Best All preschool children After this, it is usually too late for occlusion therapy Illiterate "E" chart a.k.a. "Home Eye Test." < 4y/o Photorefraction useful in screening for anisometropia, ametropia, astigmatism, and strabismus in preschool children This was a retrospective consecutive case series analysis of children treated for amblyopia at a tertiary care center. All children received full time occlusion (FTO) for the dominant eye. Results: Eighty-eight children older than 6 years at the time of initiation of therapy were included. Age at initiation of therapy ranged from 6 to 20 years (9.45 ± 3.11 years). Forty-two children (47.7%) had strabismic amblyopia, 37 (42.0%) had anisometropic amblyopia and 9 (10.2%) had a combination of strabismic and anisometropic amblyopia. Eighty out of 88 eyes (90.0%) had improvement in visual acuity following FTO. Visual acuity (VA) improved from 0.82 ± 0.34 at presentation to 0.42 ± 0.34 ( P < 0.001) after FTO. In children with strabismic amblyopia, VA improved from 0.81 ± 0.42 to 0.42 ± 0.39 ( P < 0.001). In children with anisometropic amblyopia, visual acuity of the amblyopic eye improved from 0.82 ± 0.24 to 0.36 ± 0.29 ( P < 0.001) following FTO. Out of 13 children older than 12 years, only 6 children (46.1%) had improvement in VA. Mean follow-up after complete stoppage of occlusion was 8.37 ± 1.78 months. Conclusion: Occlusion therapy yields favorable results in strabismic and/or anisometropic amblyopia, even when initiated for the first time after 6 years of age. After 12 years of age, some children may still respond to occlusion of the dominant eye. photorefraction A family of photographic techniques that provide a rapid, objective method of measuring the refractive error and accommodative response of the eye. Light emitted from a small flash source placed close to the camera lens is reflected from the eye and returned to the camera. Three methods have been developed: orthogonal, isotropic and eccentric (also called photoretinoscopy). The optical design of each method results in a specific photographic pattern, which varies with the degree to which the eye is defocused with respect to the plane of the camera. Photorefractive methods are not as accurate as retinoscopy but as they are entirely objective, much quicker and do not require prolonged fixation on the part of the patient, they are highly suited for testing infants and young children. See optometer; refractive error;retinoscope.

Prevention of Ocular Damage Due to Systemic Diseases
Diabetic Retinopathy Most common cause of blindness – 20-64y/o Must undergo regular fundal examination New vessel formation on the optic disk and exudates around the macula Any diabetic developing visual loss should also be referred for ophthalmic assessment. Control your blood sugar levels. Long-term studies show that keeping blood sugar levels in a target range reduces the risk of the development and progression of retinopathy.1 Keep blood sugar levels in a target range by eating a healthful diet, frequently monitoring your blood sugar levels, getting regular physical exercise, and taking insulin or medicines for type 2 diabetes if prescribed. One study found that teens who kept their blood sugar levels in a target range reduced their risk for diabetic retinopathy and also reduced kidneydamage during young adulthood.2 Control your blood pressure. Long-term studies suggest that retinopathy is more likely to progress to the severe form and that macular edema is more likely to occur in people who have high blood pressure. It is not clear whether treating high blood pressure can directly affect long-term vision. But in general, keeping blood pressure levels in a target range can reduce the risk of many different complications of diabetes.1 For more information about how to control your blood pressure, see the topic High Blood Pressure (Hypertension). Have your eyes examined by an eye specialist (ophthalmologist or optometrist) every year. If you are at low risk for vision problems, your doctor may consider follow-up exams every 2 to 3 years. Screening for diabetic retinopathy and other eye problems will not prevent diabetic eye disease, but it can help you avoid vision loss by allowing for early detection and treatment. See an ophthalmologist if you have changes in your vision. Changes in vision-such as floaters, pain or pressure in the eye, blurry or double vision, or new vision loss-may be symptoms of serious damage to your retina. In most cases, the sooner the problem can be treated, the more effective the treatment will be. The risk of developing severe retinopathy and vision loss may be even less if you: Reduce high cholesterol. It is not known whether reducing high cholesterol levels directly affects the progression of retinopathy and vision loss, but some studies suggest that high cholesterol may increase the risk of vision loss in people with diabetes.3 Don't smoke. Although smoking has not been proved to increase the risk of retinopathy, smoking may aggravate many of the other health problems faced by people with diabetes, including disease of the small blood vessels. Avoid hazardous activities. Certain physical activities, like weight lifting or some contact sports, may trigger bleeding in the eye through impact or increased pressure. Avoiding these activities when you have diabetic retinopathy can help reduce the risk of damage to your vision. Get adequate exercise. Exercise helps keep blood sugar levels in a target range, which can reduce the risk of vision damage from diabetic retinopathy.4Talk to your doctor about what kinds of exercise are safe for you.

Diabetic Retinopathy Begin having eye examinations as follows:
Children older than 10 years who have had diabetes for years or more Adults and adolescents with type 2 diabetes soon after diagnosis Adolescents and adults with type 1 diabetes within 5 years of diagnosis After the first exam, most patients should have a yearly eye exam.

Uveitis Associated with Juvenile RA Generally asymptomatic in its early stages Often remains undetected until severe loss of vision due to glaucoma, cataract, or band keratopathy has already occurred Regular ophthalmic screening Particularly in girls with a pauciarticular onset of the disease and circulating ANA Oligoarticular Oligoarticular (or pauciarticular) JIA affects 4 or fewer joints in the first 6 months of illness. Oligo means few. Oligoarticular is used with JIA terminology, and pauciarticular is used with JRA terminology.[17] Patients with oligoarticular JIA are more often ANA positive, when compared to other types of JIA.[18] Accounts for about 50% of JIA cases. Usually involves the knees, ankles, and elbows but smaller joints such as the fingers and toes may also be affected. The hip is not affected unlike polyarticular JIA. It is usually not symmetrical, meaning the affected joints are on one side of the body rather than on both sides simultaneously. Children with pauciarticular JRA are at risk for developing a chronic iridocyclitis or an anterior uveitis, which is inflammation of the eye. This condition often goes unnoticed; therefore these children should be closely monitored by an ophthalmologist or optometrist, generally involving 6 monthly examination under a slit-lamp.[19]

Xerophthalmia/Keratomalacia Vitamin A deficiency disease Poverty 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 GI disease such as chronic diarrhea Measles may result in severe corneal disease. Xerophthalmia, for dry eyes, is a medical condition in which the eye fails to produce tears. It may be caused by a deficiency in vitamin A and is sometimes used to describe that lack, although there may be other causes. Xerophthalmia caused by a severe vitamin A deficiency is described by pathologic dryness of the conjunctiva and cornea. Theconjunctiva becomes dry, thick and wrinkled. If untreated, it can lead to corneal ulceration and ultimately to blindness as a result of corneal damage. Keratomalacia is an eye disorder that leads to a dry cornea. One of its major causes is Vitamin A deficiency

Xerophthalmia/Keratomalacia Eye signs Night Blindness Bitot's Spots Lackluster Corneal Epithelium Blindness - secondary infection and corneal perforation Large IM doses of vitamin A, corrective diet, careful analysis of all possible causes Bitot's spots are the buildup of keratin debris located superficially in the conjunctiva, which are oval, triangular or irregular in shape. These spots are a sign of vitamin A deficiency and are associated with conjunctival xerosis. Xerosis - dry

Prevention of Visual Loss Due to Drugs
Ophthalmic drugs Packaged and labeled Color-labeling Patient should bring along any previously prescribed medications in order to avoid duplication and possible overdosage Special monitoring and special warnings to the patient

Atropine and scopolamine, used to dilate the pupil in iridocyclitis Acute glaucoma in patients with narrow anterior chamber angles Prolonged use - conjunctivitis and allergic eczema of the eyelids Preservatives in eye drops Commonly the cause of allergic reactions and Prolonged use - cicatrizing conjunctivitis similar to cicatricial pemphigoid Topical anesthetics Prolonged use - severe corneal ulceration and scarring Topical atropine is used as a cycloplegic, to temporarily paralyze the accommodation reflex, and as a mydriatic, to dilate the pupils. Atropine degrades slowly, typically wearing off in 7 to 14 days, so it is generally used as a therapeuticmydriatic, whereas tropicamide (a shorter-acting cholinergic antagonist) or phenylephrine (an α-adrenergic agonist) is preferred as an aid to ophthalmic examination. Atropine induces mydriasis by blocking contraction of the circularpupillary sphincter muscle, which is normally stimulated by acetylcholine release, thereby allowing the radial pupillary dilator muscle to contract and dilate the pupil. Atropine induces cycloplegia by paralyzing the ciliary muscles, whose action inhibits accommodation to allow accurate refraction in children, helps to relieve pain associated with iridocyclitis, and treats ciliary block (malignant) glaucoma. Atropine is contraindicated in patients pre-disposed to narrow angleglaucoma. Atropine can be given to patients who have direct globe trauma.

Corticosteroids Drop or ointment forms Depress the local defense mechanisms and precipitate corneal infection May also worsen herpetic keratitis Prolonged use - open-angle glaucoma and posterior subcapsular cataract HSV and VZV corneal infections

Systemic Drugs Keratopathy Retrobulbar neuritis Retinopathy Stevens-Johnson Syndrome (erythema multiforme) Careful history-taking Optic Neuritis Definition Optic neuritis is a vision disorder characterized by inflammation of the optic nerve. Description Optic neuritis occurs when the optic nerve, the pathway that transmits visual information to the brain, becomes inflamed and the myelin sheath that surrounds the nerve is destroyed (a process known as demyelination). It typically occurs in one eye at a time (70%), and the resulting vision loss is rapid and progressive, but only temporary. Thirty percent of patients experience occurrence in both eyes. Optic neuritis tends to afflict young adults with an average age in their 30s. Seventy-five percent of patients with optic neuritis are women. Nerve damage that occurs in the section of the optic nerve located behind the eyeball, is called retrobulbar neuritis, and is most often associated with multiple sclerosis. Optic nerve inflammation and edema (swelling) caused by intracranial pressure at the place where the nerve enters the eyeball is termed papillitis. Causes and symptoms Symptoms of optic neuritis include one or more of the following: blurred or dimmed vision blind spots, particularly with central vision pain with eye movement headache sudden color blindness impaired night vision impaired contrast sensitivity Sjs 1 - corneal neovascularization and conjunctivalization of the ocular surface. Sjs 2 - Epithelial defect of the cornea with neovascularization and surface conjunctivalization Red eye Tearing Dry eye Pain Blepharospasm Itching Grittiness Heavy eyelid Foreign body sensation Decreased vision Burn sensation Photophobia Diplopia

Methodology: 5 year randomised clinical trial
798 subjects randomised into treatment and control groups, years old best corrected visual acuity (BCVA) of 20/40 or better in both eyes No history of diabetes mellitus, intraocular surgery, radiation therapy, corticosteroid therapy, or active use of vitamin supplements.

Intervention: Beta-carotene, C and E supplementation, three times weekly
Primary variable: change in nuclear opalescence (slit- lamp grading) Annual examinations were performed for each subject by three examiners, in a masked fashion.

A Randomized, Double-Masked, Placebo Controlled Clinical Trial of Multivitamin Supplementation for Age-Related Lens Opacities: Clinical Trial of Nutritional Supplements and Age Related Cataract

Subjects: Events: 1020 patients, 55-70 yo with early or no cataract
Intervention: daily multivitamins/mineral (Centrum) Control: Nothing Followed up for 9.0 +/- 2.4 years Events: Cataract surgery Nuclear opacity: increase from baseline Cortical opacity: 10% increase in area within a standard central 5-mm circle of the lens from baseline Posterior subscapular opacity: 5% increase in area

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Preventive OpHthalmology

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