sign in sign up
<<
Home , Amaurosis fugax, Band keratopathy, Conjunctivitis, Episcleritis, Exophthalmos, Hypopyon

COVER ARTICLE

Ocular Manifestations of Autoimmune SAYJAL J. PATEL, LT, MC, USNR and DIANE C. LUNDY, CAPT, MC, USN Naval Medical Center, San Diego, California

Rheumatoid arthritis, juvenile , Sjögren’s syndrome, the seronegative , systemic erythematosus, , , and Graves’ disease are autoimmune disorders commonly encountered by family physi- cians. These autoimmune disorders can have devastating systemic and ocular effects. Ocu- lar symptoms may include dry or , foreign-body sensation, pruritus, , , visual changes, and even complete loss of vision. Because a number of these may initially present with ocular symptoms, physicians should maintain a high index of sus- picion to make a timely diagnosis. A thorough ophthalmic examination, including , pupillary reaction, ocular motility, confrontation field testing, external inspection, and direct ophthalmoscopy with fluorescein staining, should be completed. In the patient with the complaint of a “dry ” or a “,” simple tools such as the Schirmer’s test or the blanching effect of can be useful in diagnosis. In general, managing the systemic effects with nonsteroidal anti-inflammatory drugs, , and immuno- suppressive agents controls the ocular symptoms. When visual function is threatened, sur- gical therapy may be necessary. Early and accurate diagnosis with prompt treatment or referral to an ophthalmologist may prevent systemic and ocular disabilities. (Am Fam Physi- cian 2002;66:991-8. Copyright© 2002 American Academy of Family Physicians.)

atients with autoimmune such as choroiditis, retinal , epis- diseases are frequently en- cleral nodules, retinal detachments, and countered by family physi- .1,2 cians. It is important to un- sicca, or dry eye derstand not only the systemic syndrome, is the most common ocular Peffects of these diseases but also their manifestation of RA and has a reported ocular manifestations (Table 1).Most prevalence of 15 to 25 percent.1,2 Symp- ocular complications involve the toms are historically more prominent but may also include the , during the latter part of the day because of , , , and surrounding the evaporation of the tear film (Table 2). structures (Figure 1).The majority of A simple and easy-to-perform test assess- these diseases will ultimately need to be ing the function of the lacrimal glands is referred to an ophthalmologist. the Schirmer’s test (Figure 2).It is per- formed by first drying the tear film, then Rheumatoid Arthritis inserting a Schirmer strip into the lower Approximately 25 percent of patients conjunctival cul-de-sac toward the tem- with rheumatoid arthritis (RA) will have poral aspect of the lower lid. No anes- See page 937 for definitions ocular manifestations. These may in- thetic should be used. After five minutes, of strength-of-evidence levels contained in this clude keratoconjunctivitis sicca, , if the strip measures less than 10 mm of article. , , peripheral corneal wetting, the lacrimal glands are not func- ulceration, and less common entities tioning correctly. If a is available, corneal examination may reveal punctate erosive keratopathy or filaments.3,4 Approximately 25 percent of patients with rheumatoid arthritis have The primary goal in managing dry eye is to replenish or preserve the tear film. ocular manifestations, most commonly keratoconjunctivitis sicca. Patients should be educated about simple measures such as using and

SEPTEMBER 15, 2002 / VOLUME 66, NUMBER 6 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 991 TABLE 1 Ocular Manifestations of

Disease Ocular manifestations Disease Ocular manifestations

Rheumatoid arthritis Keratoconjunctivitis sicca, scleritis, Giant cell arteritis , , episcleritis, keratitis, ulcerative vision loss keratitis, choroiditis, retinal vasculitis, Graves’ disease Proptosis/, lid lag episcleral nodules, retinal detachments, and retraction, keratitis, macular edema decreased visual acuity, Juvenile rheumatoid arthritis reduced visual fields, Sjögren’s syndrome Keratoconjunctivitis sicca relative afferent pupillary Uveitis defect, loss of color vision Reiter’s syndrome , uveitis, keratitis Myasthenia gravis Diplopia, Enteropathic arthritis Uveitis, episcleritis, peripheral Uveitis, conjunctival nodules, ulcerative keratitis cranial nerve palsies, enlarged Uveitis, conjunctivitis, keratitis lacrimal glands, optic Systemic lupus Keratoconjunctivitis sicca, neuropathy erythematosus conjunctivitis, uveitis, episcleritis, Wegener’s granulomatosis Proptosis/exophthalmos, orbital scleritis, keratitis, retinal hemorrhages, cellulitis, uveitis, corneal retinal vasculitis, proliferative ulcers, , optic , Behçet’s syndrome Uveitis, ischemic optic neuropathy, Antiphospholipid Vaso-occlusive retinopathy, hemianopia, amaurosis, internuclear syndrome ischemic optic neuropathy ophthalmoplegia, pupillary Episcleritis, scleritis, optic abnormalities, oculomotor neuropathy abnormalities, visual hallucinations Takayasu’s arteritis Vaso-occlusive retinopathy, Multiple sclerosis Afferent: , ischemic optic neuropathy, retrobulbar neuritis, defects Efferent: internuclear ophthalmoplegia, Dermatomyositis Eyelid/conjunctival edema, dysmetria, , cranial retinopathy, uveitis nerve palsies

room humidifiers, and avoiding dry environ- Anterior chamber ments before turning to tear substitutes. Nat- Cornea ural or artificial tear substitutes can help allevi- Conjunctiva . . ate more severe symptoms, but most contain . 5 Limbus preservatives that can be toxic to the cornea. In Posterior . . severe cases, occlusion of the lacrimal drainage chamber . Schlemm’s . . . puncta or will be necessary. . . canal Zonules . . Sclera . . Retina Central retinal . . . artery and vein Vitreous cavity . Dura mater . . Fovea . Macula ILLUSTRATION BY CHRIS GRALAPP FIGURE 1. Cross section of the eye. Redrawn with permission from Bradford CA. Basic for medical students and primary care residents. 7th ed. San Francisco: American Academy FIGURE 2. The Schirmer’s test is used to assess of Ophthalmology, 1999. the function of the lacrimal glands.

992 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 66, NUMBER 6 / SEPTEMBER 15, 2002 Ocular Disease

tion of the can help differentiate the two. After asking the patient to look down with eye- lids closed, the physician gently presses the globe. Patients with scleritis have tenderness on palpation, while those with episcleritis do not. FIGURE 3. Scleritis. Engorged scleral vessels do Topical phenylephrine 2.5 percent (Neo- not blanch with application of topical Synephrine) can help the physician distin- phenylephrine 2.5 percent. guish dilated vessels caused by scleritis from those caused by episcleritis. The instillation of one to two drops in the affected eye will cause the engorged vessels caused by episcleritis to blanch while those caused by scleritis remain dilated. Patients should be warned that phenylephrine will cause and dilation of the pupil for approximately three hours. This test should not be done in patients with a history of . Among the variations of scleritis, necrotiz- ing scleritis with is the most destructive. In addition to the ocular findings in non-necrotizing scleritis, avascular areas of the sclera or may be seen, surrounded FIGURE 4. Episcleritis. Engorged episcleral ves- by scleral edema (Figure 5).Complications sels give the eye a bright red appearance. include scleral thinning, staphyloma, or perfo- Blanching of the vessels occurs with applica- 1,7 tion of topical phenylephrine 2.5 percent. ration. Necrotizing scleritis without inflam- mation is a sign of long-standing RA and can lead to scleromalacia perforans (Figure 6). Between the two forms of episcleritis, sim- ple episcleritis is more common in patients with RA. The presence of subconjunctival

FIGURE 5. Necrotizing scleritis (left) and scleri- tis (right). Note the avascular areas of sclera surrounded by edema (arrow).

Scleritis (Figure 3) or episcleritis (Figure 4) in patients with RA occurs at a prevalence rate of 4 to 10 percent.1 RA is the most common cause of scleritis, accounting for approximately 18 to 33 percent of cases.1,2,6 Scleritis and epis- cleritis are distinguished on the basis of 1,2,7 anatomy and appearance (Table 2).Symp- FIGURE 6. Scleromalacia perforans. Note the toms may be similar, but the pain in scleritis is thinning of the sclera, which leaves the choroid more evident and severe. Tenderness to palpa- bare and covered by a thin layer of conjunctiva.

SEPTEMBER 15, 2002 / VOLUME 66, NUMBER 6 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 993 TABLE 2 Ocular in Autoimmune Disease

Condition Symptoms Signs Treatment

Keratitis Pain with photophobia, foreign Inflammatory cell infiltrate, corneal NSAIDs, topical/oral/IV steroids, body sensation, tearing, red opacification, corneal vascularization, immunosuppressives, surgery eye, decreased vision corneal ulceration Keratoconjunctivitis Dry eye, burning, pain, blurred Diminished corneal tear meniscus, Sunglasses, room humidifiers, sicca vision, pruritus, foreign-body abnormal Schirmer’s test tear substitutes, surgery sensation, mucous threads and crusting about the Scleritis Gradual onset; deep, boring Decreased visual acuity; bluish appearance NSAIDs, topical/oral/IV steroids, pain may radiate into cheek, with engorged blood vessels; may have immunosuppressives, surgery eyebrows, and temples; immovable, tender nodules over the blurred vision; photophobia sclera, general tenderness on palpation; engorged blood vessels do not blanch with phenylephrine (Neo-Synephrine); avascular areas over the sclera Episcleritis Sudden onset; mild ache may No change in visual acuity; bright red NSAIDs, topical/oral steroids radiate into cheek, eyebrows, appearance with engorged blood and temples; no blurred vessels; may have movable, nontender vision; photophobia nodules over the episclera; no tenderness on palpation; engorged blood vessels blanch with phenylephrine Uveitis Red eye, pain, photophobia, Decreased visual acuity, inflammatory Cycloplegics, topical steroids, blurred vision infiltrate in the anterior chamber, immunosuppressives synechiae, pupillary Optic neuritis Visual loss, pain with eye Decreased visual acuity, loss of color IV steroids with positive MRI movement, photophobia vision, central , afferent pupillary findings defect, swollen optic nerve Exophthalmos Irritable and gritty eyes, double Protruding globe, widened palpebral Lubricating eye drops, sleeping or blurred vision, photophobia, fissures, conjunctival injection and with head elevated, sunglasses, increased tearing, orbital , lid lag and retraction, exposure eyelid taping at night, steroids, pressure keratitis radiotherapy, surgery

NSAIDs = nonsteroidal anti-inflammatory drugs; IV = intravenous; MRI = magnetic resonance imaging.

nodules that are mobile over the sclera differ- who do not respond to these entiates nodular episcleritis from simple epis- should be referred to an ophthalmologist for cleritis.1,7 Both forms of episcleritis can be possible treatment with topical steroids or sys- confused with severe conjunctivitis because of temic immunosuppressive medications. the bright-red appearance of the eye and Corneal disease in patients with RA can be should be differentiated with the help of a an isolated , but it is most com- thorough history and . monly associated with keratoconjunctivitis The importance of correctly diagnosing and sicca or a form of anterior scleritis. The spec- distinguishing between scleritis and episcleritis trum of disease may include keratitis, scleros- is based on the potential ocular and systemic ing keratitis, and peripheral or paracentral complications associated with scleritis. Studies ulcerative keratitis1,2,6,7 (Table 2).The drying have shown that patients with RA-associated effects of keratoconjunctivitis sicca lead to scleritis have more widespread systemic dis- devitalized epithelial cells and punctate ease and a higher mortality rate than those epithelial erosions. Keratitis associated with without scleritis.6-8 The initial treatment of scleritis may be acute or sclerosing. Acute ker- scleritis and episcleritis should be focused on atitis has been identified in 30 to 70 percent of relieving discomfort and stopping progression patients with scleritis or episcleritis-associated of the disease. Initial therapy includes oral RA.1,6 It is marked by an inflammatory cell indomethacin (Indocin) or other nonsteroidal infiltrate that may result in corneal scarring, anti-inflammatory drugs (NSAIDs). Patients ulceration, or melting.1,6

994 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 66, NUMBER 6 / SEPTEMBER 15, 2002 FIGURE 8. Corneal perforation. Severe tear deficiency leads to breakdown of the corneal epithelial layer.

FIGURE 7. Peripheral corneal ulceration. Note the crescent-shaped destructive inflammation of the juxtalimbal cornea.

Sclerosing keratitis is a chronic process marked by an area of opacified and vascular- ized cornea that progresses toward the visual axis. This area of opacification may be more evident with fluorescein staining. Peripheral and paracentral ulcerative keratitis can occur in association with, or in the absence of, scle- ritis and are marked by corneal thinning in the juxtalimbal cornea (peripheral) or the central (paracentral) cornea1,2 (Figure 7).Without FIGURE 9. Posterior synechiae caused by adhe- treatment, perforation (Figure 8) and visual sion of the iris to the lens, resulting in an irregularly shaped pupil. loss may occur. Care must be taken when pre- scribing steroids to prevent further thinning of the cornea. It is important that the patient tom-free or have blurred vision (Table 2).On receive a thorough ocular examination with examination, the patient may have decreased frequent slit lamp follow-up evaluations. Typ- visual acuity, , synechiae (Fig- ically, topical steroids, immunosuppressive ure 9), cataracts, or elevated ocular pressure. therapy, surgical intervention, or a combina- Diagnosis or suspicion of juvenile RA should tion of the above will be required to preserve prompt a referral to a pediatric ophthalmolo- vision. Surgical options include ulcer debride- gist. Recommendations for ocular screening ment, conjunctival resection, corneal graft, examinations are based on the risk of develop- application of tissue adhesives, sclerectomy, ing uveitis (Table 3).10 Therapy involves close and scleral patch grafting.1,2,8 monitoring by an ophthalmologist, with the Other, less common ocular manifestations use of cycloplegic agents, steroids, NSAIDs, or of RA include choroiditis, retinal vasculitis, immunosuppressive agents.1,2 episcleral nodules, exudative or serous retinal detachments, and macular edema.1,2,6 A high Sjögren’s Syndrome index of suspicion can preserve vision and The primary ocular manifestation of Sjö- prevent further ocular complications. gren’s syndrome is keratoconjunctivitis sicca. The signs and symptoms are similar to those Juvenile Rheumatoid Arthritis of keratoconjunctivitis sicca associated with Juvenile rheumatoid arthritis accounts for RA. In addition to the treatment noted above, approximately 80 percent of cases of uveitis in 5 mg of oral pilocarpine (Salagen) four times children.1,2,9 Delay in diagnosis can lead to daily may improve the symptoms of dry eyes cataracts, glaucoma, and blindness. Although and dry mouth.11,12 [Reference 11, Evidence uveitis can be found in all forms of juvenile level A, randomized controlled trial ] Patients RA, it is most commonly found in the pauci- should be cautioned that the side effects of articular subtype. Most patients will be symp- diaphoresis and poor night vision may occur.

SEPTEMBER 15, 2002 / VOLUME 66, NUMBER 6 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 995 enteropathic arthritis (arthritis associated with TABLE 3 Crohn’s disease or ).2,13-15 Ocu- JRA Risk Categories for Developing Uveitis lar symptoms can be unilateral or bilateral, and and Recommended Ocular Examinations pain is caused by ciliary spasm in response to anterior chamber inflammation. As noted ear- Risk Recommendations lier, patients suspected of having uveitis should High: should have ocular Pauci- or polyarticular arthritis; positive be referred to an ophthalmologist. Complica- examination every three months for antinuclear antibodies tions include glaucoma, cataracts, or blindness. Onset of arthritis ≤ 7 years Duration of arthritis ≤ 4 years Systemic Moderate: should have ocular Pauci- or polyarticular arthritis; positive Ocular disease occurs in 20 percent of examination every six months for antinuclear antibodies patients with systemic lupus erythematosus Onset of arthritis ≤ 7 years Duration of arthritis > 4 years (SLE). In some cases, ocular disease may indi- Low: should have ocular Pauci-, polyarticular, or systemic arthritis; cate reactivation of SLE that was thought to be examination every 12 months negative for antinuclear antibodies in remission.16 External ocular manifestations Onset of arthritis > 7 years include keratoconjunctivitis sicca, conjunc- Duration of arthritis > 4 years tivitis, uveitis, episcleritis, scleritis, keratitis, and a discoid lupus rash over the eyelids that JRA = juvenile rheumatoid arthritis. is often confused with .16,17 Neuro- Adapted with permission from American Academy of Pediatrics, Subcommittees ophthalmic involvement in SLE is primarily of Rheumatology and Ophthalmology. Guidelines for ophthalmic examinations caused by microinfarction, hemorrhage, or in children with juvenile rheumatoid arthritis. Pediatrics 1993;92:295-6. vasculitis in various locations of the eye and along the visual pathway. Typical complica- tions include optic neuritis, ischemic optic Spondyloarthropathies neuropathy, hemianopia, amaurosis, internu- Among the seronegative spondyloarthrop- clear ophthalmoplegia, pupillary abnormali- athies, uveitis in ankylosing spondylitis is the ties, oculomotor abnormalities, pseudotumor most common ocular manifestation. It occurs cerebri, and visual hallucinations.16 in approximately 25 percent of patients with Retinal disease primarily occurs in patients ankylosing spondylitis, in up to 37 percent of with active SLE and may include cotton-wool patients with Reiter’s syndrome, in approxi- spots (Figure 10),retinal hemorrhages, retinal mately 20 percent of patients with psoriatic vasculitis, or proliferative retinopathy. Treat- arthritis, and in up to 9 percent of patients with ment of ocular disease is based on specific pathology and underlying disease.16 Kerato- conjunctivitis sicca is thought to be the most common manifestation and can be treated as The Authors noted above. Retinal disease has a high morbidity and SAYJAL J. PATEL, LT, MC, USNR, is an ophthalmology resident at Naval Medical Cen- ter, San Diego. He received his medical degree from Jefferson Medical College of should be treated aggressively by an ophthal- Thomas Jefferson University, Philadelphia. mologist.16,17 Ophthalmic screening pro- DIANE C. LUNDY, CAPT, MC, USN, is currently serving as Director of the Glaucoma Ser- grams in SLE are controversial. Most physi- vice at Naval Medical Center, San Diego. She received her medical degree from the Uni- cians agree that patients on antimalarial or formed Services University of the Health Sciences F. Edward Hébert School of Medicine, steroid regimens should receive a full Bethesda, Md. She completed an ophthalmology residency at Naval Medical Center, San Diego, and a glaucoma fellowship at the Doheny Eye Institute, Los Angeles. dilated-eye examination on initiation of therapy then with routine examinations in Address correspondence to Lt. Sayjal J. Patel, 34520 Bob Wilson Dr., San Diego, CA 92134-2202 (e-mail: [email protected]). Reprints are not available from low-risk patients and yearly for high-risk the authors. patients. High risk is defined by

996 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 66, NUMBER 6 / SEPTEMBER 15, 2002 Ocular Disease

Ocular disease may occur in 50 percent of patients with giant cell arteritis and is commonly present in patients who are still without systemic signs or symptoms.

Giant Cell Arteritis Up to 50 percent of patients with giant cell arteritis present with ocular symptoms that include pain, diplopia, visual loss, and amauro- sis fugax, in addition to , jaw claudica- tion, and neck pain.21,22 It is important to note FIGURE 10. Cotton-wool spots in a patient with systemic lupus erythematosus. that ocular involvement is common in the absence of systemic signs and symptoms.21,22 Patients may have temporal artery tenderness dosage (>6.5 mg per kg hydroxychloroquine or a decreased temporal artery pulse, but diag- or >3 mg per kg chloroquine), duration of nosis is confirmed with biopsy of the artery and use (more than five years), high body fat elevated titers of erythrocyte sedimentation level, presence of renal or liver disease, pres- rate and C-reactive protein. Biopsy will remain ence of concomitant retinal disease, and age positive for up to two weeks after the initiation greater than 60 years.16,18 of therapy.21 Intravenous corti- costeroids should be used in patients with Multiple Sclerosis visual symptoms.21 Immediate therapy can be The ocular manifestations of multiple sclero- dramatic in effect and prevent further vasculitic sis (MS) can be divided into afferent and effer- complications, permanent blindness, or death. ent disorders19 (Table 1).Optic neuritis is diag- nosed in 75 percent of patients with MS and is Graves’ Disease the presenting symptom in 14 to 25 percent of Exophthalmos (Figure 11) occurs in ap- cases19,20 (Table 2).Visual field defects in proximately 50 percent of patients with thy- patients with MS are a result of demyelination roid disease23 (Table 2).It is strongly associ- along the visual pathway. Bilateral internuclear ated with smoking and may also be found in ophthalmoplegia is almost always caused by a patients who are euthyroid or hypothyroid.23 demyelinating disorder.19 Dysmetria, nystag- If signs of optic nerve compression, such as mus, and cranial nerve palsies, especially decreased visual acuity, reduced visual fields, involving the sixth and third nerves, may result from lesions of the stem and . Nystagmus, which may be the first neuro- The rightsholder did not logic finding in patients with MS, is com- grant rights to reproduce monly horizontal but may also be rotary or this item in electronic 19 vertical. Patients with suspected ocular media. For the missing involvement should receive magnetic reso- nance imaging (MRI), a full dilated-eye exam- item, see the original print ination, and treatment with intravenous corti- version of this publication. costeroids if the MRI is positive.20 Periodic follow-up evaluations should be done to FIGURE 11. monitor the progression of disease.

SEPTEMBER 15, 2002 / VOLUME 66, NUMBER 6 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 997 Ocular Disease

relative afferent pupillary defect, and loss of Buchanan WW, Dick WC, et al. Episcleritis and scleritis. A study of their clinical manifestations and color vision are present, computed tomogra- association with rheumatoid arthritis. Br J Ophthal- 23-25 phy or MRI of the is recommended. mol 1976;60:192-226. Patients with suspected ocular disease 7. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol 1976;60:163-91. should be referred to an ophthalmologist for a 8. Messmer EM, Foster CS. Destructive corneal and full dilated ocular examination. Mild ocular scleral disease associated with rheumatoid arthritis. disease can be treated with simple methods Medical and surgical management. Cornea 1995; 14:408-17. such as lubrication drops applied hourly, 9. Waheed NK, Miserocchi E, Foster CS. Ocular con- sleeping with the head elevated, wearing sun- cerns in juvenile rheumatoid arthritis. Int Ophthal- glasses during the daytime, and taping eyelids mol Clin 2001;41:223-34. 10. American Academy of Pediatrics. Guidelines for closed at night. Systemic corticosteroid therapy ophthalmic examinations in children with juvenile or radiotherapy is reserved for more severe rheumatoid arthritis. Pediatrics 1993;92:295-6. cases, and surgical decompression of the orbit 11. Vivino FB, Al-Hashimi I, Khan Z, LeVeque FG, Salis- bury PL 3d, Tran-Johnson TK, et al. Pilocarpine or tarsorrhaphy may be required in patients tablets for the treatment of dry mouth and dry eye with sudden visual loss or extensive corneal symptoms in patients with Sjögren syndrome: a damage, respectively.23,25 randomized, placebo-controlled, fixed-dose, multi- center trial. Arch Intern Med 1999;159:174-81. 12. Manoussakis MN, Moutsopoulos HM. Sjögren’s Figure 1 redrawn with permission from Bradford syndrome. Otolaryngol Clin North Am 1999;32: CA. Basic ophthalmology for medical students and 843-60. primary care residents. 7th ed. San Francisco: Amer- 13. Rosenbaum JT. Acute anterior uveitis and spondy- ican Academy of Ophthalmology, 1999, and the loarthropathies. Rheum Dis Clin North Am 1992; photographs in Figures 3 through 8, 10, and 11 are 18:143-51. used with permission from Tang RA. Ocular mani- 14. Bañares A, Hernández-García C, Fernández-Gutiér- festation of systemic disease. San Francisco: Ameri- rez B, Jover JA. Eye involvement in the spondy- can Academy of Ophthalmology, 1996. loarthropathies. Rheum Dis Clin North Am 1998; 24:771-84. 15. Lyons JL, Rosenbaum JT. Uveitis associated with The authors indicate that they do not have any con- inflammatory bowel disease compared with uveitis flicts of interest. Sources of funding: none reported. associated with . Arch Oph- thalmol 1997;115:61-4. The opinions and assertions contained herein are the 16. Nguyen QD, Foster CS. Systemic lupus erythe- private views of the authors and are not to be construed matosus and the eye. Int Ophthalmol Clin 1998; as official or as reflecting the views of the U.S. Navy 38:33-60. Medical Department or the U.S. Navy Service at large. 17. Soo MP, Chow SK, Tan CT, Nadior N, Yeap SS, Hoh HB. The spectrum of ocular involvement in patients with systemic lupus erythematosus without ocular A list of terms and definitions is available on the Web symptoms. Lupus 2000;9:511-4. site at www.aafp.org/afp/20020915/991x.html. 18. Marmor MF, Carr RE, Easterbrook M, Farjo AA, Mieler WF. Recommendations on screening for REFERENCES chloroquine and hydroxychloroquine retinopathy. Ophthalmology 2002;109:1377-82. 1. Fuerst DJ, Tanzer DJ, Smith RE. Rheumatoid dis- 19. Kidd D. Presentations of multiple sclerosis. Practi- eases. Int Ophthalmol Clin 1998;38:47-80. tioner 1999;243:24-6,28-30. 2. Harper SL, Foster CS. The ocular manifestations of 20. Davis EA, Rizzo JF. Ocular manifestations of multi- rheumatoid disease. Int Ophthalmol Clin ple sclerosis. Int Ophthalmol Clin 1998;38:129-39. 1998;38:1-19. 21. Neff AG, Greifenstein EM. Giant cell arteritis 3. Whitcher JP Jr, Gritz DC, Daniels TE. The dry eye: a update. Semin Ophthalmol 1999;14:109-12. diagnostic dilemma. Int Ophthalmol Clin 1998;38: 22. Hayreh SS, Podhajsky PA, Zimmerman B. Ocular 23-37. manifestations of giant cell arteritis. Am J Ophthal- 4. Friedlaender MH. Ocular manifestations of Sjö- mol 1998;125:509-20. gren’s syndrome: keratoconjunctivitis sicca. Rheum 23. Weetman AP. Graves’ disease. N Engl J Med 2000; Dis Clin North Am 1992;18:591-608. 343:1236-48. 5. Geerling G, Daniels JT, Dart JK, Cree IA, Khaw PT. 24. Adam A, Mishriki YY. The painful, protruding eye. Toxicity of natural tear substitutes in a fully defined Unilateral euthyroid Graves’ ophthalmopathy. Post- culture model of human corneal epithelial cells. grad Med 1999;105:81-4. Invest Ophthalmol Vis Sci 2001;42:948-56. 25. Coday MP, Dallow RL. Managing Graves’ orbitopa- 6. McGavin DD, Williamson J, Forrester JV, Foulds WS, thy. Int Ophthalmol Clin 1998;38:103-15.

998 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 66, NUMBER 6 / SEPTEMBER 15, 2002