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Postoperative Sympathetic Ophthalmia

Alice T. Gasch, M.S., M.D. C. Stephen Foster, M.D., F.A.C.S. Cynthia L. Grosskreutz, M.D., Ph.D. Louis R. Pasquale, M.D.

Classically, but not always, sympathetic ophthalmia (SO) is a bilateral, granulomatous panuveitis that occurs after injury to the uvea of one eye. The injured eye has been termed the exciting or sympathogenic eye, and the contralateral eye has been called the sympathizing eye. The inciting injury may result not only from unintentional or intentional penetrating ocular trauma but also from nonpenetrating ocular surgery. Though uncom mon, the disease is a fearful postoperative complication because of its po tential to blind both eyes. Furthermore, SO is a thought-provoking post operative complication because probably it is unique in being a disease in which an insult to a relatively independent body organ leads to inflam matory disease elsewhere in the body. It also is an intriguing postoperative complication because its pathogenesis is an enigma. This chapter reviews the historical background, epidemiology, clinical features, histopathologic features, pathogenesis, differential diagnosis, treatment, and prognosis of SO. Emphasis is placed on SO as a postoper ative complication.

Historical Background
More than 2,000 years ago, Hippocrates taught that injury to one eye can lead to disease in the other eye;' but not until 1000 AD did the first known written reference to SO appear. It stated, "The right eye when dis eased, often gives suffering to the left.,,2.3 In the sixteenth century, the first German textbook of ophthalmology noted that after injury to one eye, "the other good eye is .. in great danger.?" Subsequently, during the eigh69

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teenth and nineteenth centuries, multiple reports cited the disease.l-f However, the first comprehensive clinical description of SO is attributed to William Mackenzie, who gave the disease its present name in 1840. In 1905, Ernest Fuchs provided the classic histopathological description of the disease.f which established SO as a distinct disease entity. Interestingly, Louis Braille who, at 16 years old, devised the writing sys tem of Braille in the early nineteenth century, is thought to have lost his sight from SO: One eye received a penetrating injury by a leather awl, and vision in the other eye gradually deteriorated 2 years later."

Assessment of the prevalence of SO is difficult, partly because it is low and partly because it has been confused with other diagnoses, particularly in the older literature. The incidence of SO associated with intraocular surgery may be less than that secondary to nonsurgical trauma. In one histopathological series of257 cases, 43% occurred after penetrating surgery." Similarly, in a sub sequent histopathological series of 99 cases, penetrating surgery accoun ted for 40.4% of cases, whereas nonsurgical penetrating trauma ac counted for 53.5%.8 In contrast, in another series of 50 cases, 10% were attributed to ocular surgery and the rest to accidental trauma or infectious perforation." Of 32 cases that presented to a uveitis clinic, 28% developed after multiple intraocular surgeries and the rest after accidental trauma.l? Studies incorporating data from the latter half of this century indicate an incidence of 0.01 to 0.05% for intraocular surgery (type of surgery not specified) 2 11-13 and of 0.28 to 1.9% for nonsurgical penetrating ocular injuries. ,13,14 Thus, the incidence of SO is low and lower after surgical than after nonsurgical injury. Surgical procedures that have been reported to incite SO include couching.l" 7 cataract extraction.v'" iridencleisis, 8,17 iridectomy,8,18,19 cyclodialysis, 2, trabeculectornyj''? vitrectomy,I,12,20,21 retinal detachment repair,22-25 evisceration.i" paracentesis," keratectorny.F''? cyclocryother apy,27-29 laser trabeculoplasry.i" neodymium:yttrium aluminum garnet (Nd:YAG) laser cyclophotocoagulation,31-34 laser retinal photocoagula tion,35 and local irradiation.Y'"? The risk of SO after vitrectomy alone is ap proximately the same as for other surgical procedures involving uveal pen etration. However, it increases when vitrectomy is associated with accidental penetrating trauma or another surgical procedure.V Interestingly, al though SO has been attributed to Nd:YAG laser cyclophotocoagula tion,31-34 it has not been reported after diode laser cyclophotocoagulation. During this century and especially during the last few decades, the in cidence of SO has decreased. 13,38-41 Explanations for this trend include Fuchs' histopathological definition of SO, which provided an objective ba-

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sis for the diagnosis.Y and improvements in both surgical techniques and management of ocular trauma. The prevalence of SO is higher in male than in female patients, but this gender difference may be attributable to a higher incidence of ocular injury in male patients. 2,s,43 This hypothesis is supported by the fact that in postsurgical cases, the incidence of SO is equal between the gen ders. 10,43 Some studies indicate that the prevalence follows the age distribution of the population.1,3,5,44,45 Other studies indicate a higher prevalence among children. 1 Yet, other studies indicate a higher prevalence among individuals older than 60 years. 7,44 The increased incidence reported for children has been attributed to a predisposition to the disease or an ele vated incidence of penetrating ocular trauma. That for individuals older than 60 might reflect their higher frequency of ocular surgery, particularly cataract extraction. 1 Generally, SO is considered not to have a predilection for race. How ever, it has been reported that the disease rarely, if ever, occurs among the Aborigines of Australia and New Zealand,46 in the Southwest Pacific,46 or in Central Africa. 47,48 If these observations are bonafide, they suggest that genetics plays a role in predisposition to the disease. Seasons unlikely affect incidence, but seasonal variation has been re ported. Two studies indicated an increased incidence in summer and spring, and two 1 studies reported a higher incidence in winter.

Clinical Features
The reported interval between ocular injury and the onset of SO ranges from 5 days 8,49 to 66 years. 50 However, the shortest reported inter val with both clinical and histopathological supportive data is 10 days.51 About 65% of cases occur 2 within 2 weeks to 2 months after injury, and about 90% occur within 1 year. ,8,4:, A prognosticator of SO is persistent inflammation of the exciting eye, sometimes leading to phthisis, despite resolution of damage from the in jury. Onset of the disease itself is insidious. Typically, the sympathizing eye initially has cyclitis, ciliary injection, pain, and photophobia. Transient hy peropia and difficulties with accommodation have been associated with early disease, presumably due to involvement of the ciliary body. Blurred vision may not occur initially but is inevitable eventually.52,53 Without adequate treatment, the disease usually progresses to granu lomatous panuveitis, which is characterized by ciliary injection, mutton-fat keratic precipitates on the corneal endothelium, aqueous cells and flare, iris thickening, posterior synechiae, vitreous cells and haze, retinal vessel sheathing, papillitis, and choroidal infiltration and thickening.V In addi tion, in approximately one third or cases, the funclus periphery exhibits

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multiple, small, yellowish-white lesions corresponding to Dalen-Fuch's nodules, 54 which is a histological finding discussed later (see Histopatho logical Features). Thus, the severity of the ocular inflammation in a patient presenting with SO may range from mild to severe. Possible sequelae include rubeosis iridis, pupillary membranes, sec ondary glaucoma, cataracts, macular edema, exudative retinal detach ment, and choroidal 52 neovascularization, as well as resultant chorioretinal scarring and phthisis. ,556o Usually, the foregoing sequelae portend a poor visual prognosis. 52 Without adequate treatment, the disease typically runs a prolonged course with recurrent episodes of painful inflammation and often even tual blindness: 2,35,58,60,61 Atypical clinical presentations have been reported in which only mild, 8 transient, nongranulomatous inflammation has occurred. ,42,59,62,63 These atypical presentations have been associated with early enucleation of the exciting 35 eye or ongoing immunosuppressive treatment. ,42,63,64 Interestingly, extraocular manifestations, though uncommon, do oc cur and include vitiligo, poliosis, alopecia, dysacusis, central nervous system symptoms consistent with irritation of the meninges (which con tain melanin), and cerebrospinal fluid pleocytosis (primarily lymphocyto sis). All these extraocular manifestations also are associated with Vogt Koyanagi-Harada (VKH) syndrome. 2,43,65 Fluorescein angiography is useful for evaluating the degree of posterior segment involvement. During acute disease, the fluorescein angiogram re flects an exudative process: It shows multiple, peripheral, subretinal spots of early hyperfluorescence that exhibit leakage and pooling as the study progresses.v" 52 Late staining of retinal vessels'i" or leakage at the optic disc (or both) may also be evident. In addition, peripheral spots of early hypo fluorescence that stain late in the study may be apparent. These hypofluo rescent SPOl'i may reflect blockage by Dalen-Fuchs nodules that have not disrupted the retinal pigment epithelium (RPE),67 or focal obliteration of the choriocapillaris, or displacement of choroidal vessels by choroidal gran ulomas (or any combination of these phenomena). Later in the disease, the fluorescein angiogram may show multiple, peripheral spots of early hyper fluorescence that fade over time and represent window defects corre sponding to mature Dalen-Fuchs nodules that have disrupted the RPE. 54 Indocyanine green angiography is useful for evaluating choroidal involvement. It shows multiple hypofluorescent dots in the intermediate phase. During the late phase, some become isofluorescent and then resolve after longterm steroid therapy, and others remain hypofluores cent. These lesions have been interpreted as being active and cicatricial, respectively.t" Electrophysiological functions were compromised in the one case of SO for which electrophysiological testing has been reported. The elec troretinogram had diminished photopic c6ne and scotopic rod b-wave

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amplitudes; the electrooculogram light peak and dark trough were ab sent; and dark adaptation testing showed elevated cone and rod thresh olds. These functions improved after treatment.P"

Histopathological Features
Apart from changes directly related to the injury, histopathological findings in both the exciting and the sympathizing eyes are similar. 2.5,43.70 The uveal tract, especially the posterior choroid, becomes thickened by a diffuse, nonnecrotizing, granulomatous inflammation (i.e., a massive lymphocytic infiltrate with interspersed granulomas composed of aggre gates of epithelioid histiocytes). Particularly in severe, untreated disease, the infiltrate may include eosinophils and plasma cells. 70-73 Phagocytosis of pigment granules by the epithelioid and giant cells occurs, which cor relates with the severity of the inflammation and with the visual outcome in the sympathizing eye. 7.8.71,72,74,75 In the sympathizing eye, lymphocyte infiltration is common along scleral emissaries, especially the vortex veins. 2.5, 73 Other classic histopathological features are relative lack of retinal in volvement, sparing of the choriocapillaris, and Dalen-Fuchs nodules.Y" DalenFuchs nodules are characteristic of SO but are not pathognomonic for the disease because they also occur in VKH syndrome 75 and in sar coidosis."? A prevalence of 25 to 36% has been reported in series of cases of SO of unspecified severity5,8,78 and in all eyes in a series of 50 cases of severe SO.9 A rule-of-thumb prevalence of one-third of cases often is stated. Dalen-Fuchs nodules are approximately 60 to 700 /-Lm in diameter and occur predominantly in the midperiphery of the fundus. They form between Bruch's membrane and the RPE, and, as they mature, may become confluent or disrupt the RPE (or both).~,!i'1,7\1 Through the early 1980s, Dalen-Fuchs nodules were thought to be RPE cells that had migrated and transformed. 5,74,80,81 However, in the mid-1980s, immunohistochemical and ultrastructural analyses revealed that these nodules are predominantly histiocytic cells, intermixed as they mature with depigmented RPE cells.",74,80,81 Thus, Dalen-Fuchs nodules and the choroidal granulomas of SO appear to be formed by cells of sim ilar origin and Iunction.Y "Atypical" histopathological features, which may appear with severe inflammaticn and advanced disease, include focal, nongranulomatous (instead of diffuse granulomatous) inflammation of the uvea,74 retinal involvement (retinitis, gliosis, perivasculitis, detachment), 7,8,71 focal oblit eration of the choriocapillaris;" choroidal scarring,"! and optic nerve inflammation and atrophy.8,9,71 Thus, like the clinical features of SO, histopathological findings of the diseaseare a varied spectrum, depending on the stage of the disease.

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Immunohistopathological studies indicate that in both classic and atypical cases of SO, the choroidal infiltrate typically is preponderantly T lymphocytes (CD3+) with B lymphocytes comprising less than 5% to 15% of the infiltrate 35,82-86 Higher prevalences of B cells have been attributed to end-stage of the disease or a second pathological process." In general, Thelper-inducer (CD4+) lymphocytes predominate early, and T-sup presser82 cytotoxic (CDS+) cells predominate later. Thus, immuno histopathological findings suggest that delayed hypersensitivity, which T cells mediate, is involved in the pathogenesis of 50. 83.87

Though infectious etiologies (implicating Mycoplasma 88 and viru ses 89,90) have been proposed, the cause of SO is unknown. Currently, the predominant hypothesis is that a penetrating injury to one eye creates conditions that allow an immune reaction to be generated against a uveal self-antigen. The occurrence of vitiligo, poliosis, and dysacusis in some pa tients suggests a generalized sensitization against melanin pigment-con taining tissues in some cases. As early as 1910, Elschnig'" proposed an au toimmune etiology. Nearly 40 years later, Collins 92,93 produced an ocular inflammation resembling SO by sensitizing guinea pigs with whole uvea homogenate in adjuvant. Intensive study ensued to determine the antigen in the homogenate. For a while, reports of sensitization with uveal tissue were thought to be attributed to contamination of uveal preparation with immunogenic retinal proteins. Three had been identified (S-antigen, in terphotoreceptor-binding protein [IRBP], and rhodopsin) ,94-97 and one (IRBP) induced a disease in monkeys that was similar histopathologically to 50. 98 99 However, at the turn of this decade, Broekhuyse and coworkers ,lOO described a partially purified uveal melanin preparation that produces an inflammation limited to the uvea in immunized animals. Chan and asso ciates 101 subsequently reported that spontaneous recurrence of inflam mation occurs in this model. Subsequently, Sugita and colleaguesl'" sug gested that in HLA-A2-positive patients, both SO and VKH may be autoimmune diseases directed toward the MART-1 peptide of melano cytes. Because SO follows uveal injury that often is not associated with reti nal involvement, a uveal antigen, rather than a retinal antigen, as the ba sis for the disorder is more consistent with clinical data. But how does the immune system become sensitized to intraocular antigens after penetrating injury? The lymphatic system of the eye to gether with work of Rao and coworkers'Y" and Roberge and associates v'" offer an explanation. Except for the conjunctiva, the eye lacks lymphat iCS. 105 Without lymphatic drainage, intraocular antigens normally are con fined to circulation in the blood and spleen, resulting in induction of sup pressor T cells. However, if intraocular antigens gain access to lymphatics,

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cell-mediated immune responses can be initiated in the regional cervical lymph nodes. 53 Independently, Rao and coworkers'Y'' in 1983 and Roberge and col leagu. _e.~104 in 1989 induced a contralateral uveitis by injecting. retinal S-anti genDlixed with adjuvant beneath the conjunctiva, but they were not able to do so by injecting this mixture into the eye. Thus, one possible scenario for induction of SO is as follows: Perforating injury allows intraocular antigens to leave their usual "immune-privileged" intraocular site via conjunctival lymphatics. Concomitantly, the injury allows adjuvant (such as endotoxin from killed skin bacteria) to enter the eye, where it can upgrade the local immune response, thereby allowing it to surpass intrinsic immunosuppres sant mechanisms in genetically predisposed individuals. 54 However, the preceding paradigm does not explain at least four phe nomena: (1) the low prevalence of SO relative to the prevalence of pene trating unintentional or intentional ocular trauma, especially filtering surgery, which exposes uveal tissue to conjunctival lymphatics; (2) the oc currence of SO after nonpenetrating ocular procedures; (3) the relative preservation of the retina and choriocapillaris in classic SO, despite ex tensive choroidal inflammation; and (4) the occasional very prolonged de lay between an inciting injury and the onset of SO. The low frequency of SO may be explained by the low prevalence of genetic predisposition. Studies have shown an association between SO and several haplotypes (HLA-Al1, -DR4, -DRw53, -DQw3, -DRB1 *04, -DQAI *03, -DQBI *04),106-109 which suggests a genetic predisposition. Both the low incidence of SO after filtering surgery and the occur rence of SO after nonpenetrating ocular procedures may be explained by the ability of aqueous to inhibit immune cell function.U" Aqueous of some inflamed eyes does not exhibit this property.i'" which has been at tributed to transforming growth factor-beta (TGF_f3)Yl,112 Evidence suggests that relative preservation of the retina and chorio capillaris could result from secretion of antiinflammatory agents by the RPE, including TGF-f3 and "retinal pigment epithelial protective protein." The latter suppresses phagocyte generation of superoxide and thereby could inhibit uveal necrosis and inflammatory cell infiltration of the retina or the choriocapillaris (or both) .113 A long delay between injury and disease might be explained by dis ruptiou of one or more im mun osupprcssivc mcch.urisms already prl'SClll or newly established at the time ofinsult.i''' For example, evidence suggests that in SO there is acquired dysregulation of apoptosis. Normally, apop tosis may facilitate limitation of ocular inflammation. 1 14

Differential Diagnosis
A history of accidental or surgical' uveal trauma is of paramount im in diagnosing SO because the clinical signs are not pathognoportance

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monic. VKH and sarcoidosis probably most closely resemble SO, but the differential sliagnosis also includes syphilis, phacoanaphylactic endoph thalmitis, arid lymphoma. Like SO, VKH, sarcoidosis, and syphilis can cause bilateral, granulomatous panuveitis. In contradistinction, pha coanaphylactic (phacoantigenic) endophthalmitis, which occurs after lens capsule disruption, typically manifests as a unilateral, severe, anterior uveitis with or without vitritis.i'" Lymphoma should be considered in older individuals with vitritis out of proportion to visual acuity,u5 In addition, patients with SO have been misdiagnosed as having multifocal choroiditis, ocular toxoplasmosis, and idiopathic anterior uveitis.l" SO and VKH have strikingly similar clinical and histopathological manifestations, including Dalen-Fuchs nodules,2.42,65,79,s7 and a high fre quency of several shared haplotypes,10S,109 The many similarities between the diseases suggest that they may involve closely related antigens and sim ilar immune mechanisms. 42,s7 However, unlike SO, in VKH, bilateral, localized, serous retinal detachments are usual,116 and systemic findings of vitiligo, poliosis, alopecia, dysacusis, and central nervous system distur bances are common. 54,l16 Also, unlike SO, VKH has fairly well-established age and ethnic group predilections (occurring most frequently during the second through fourth decades of life in Japanese, certain Latin American groups, American Indians, and African Americans.P" Furthermore, unlike VKH, a history of uveal trauma is requisite for SO. Like VKH, ocular sarcoidosis may resemble SO both clinically and histopathologically, including Dalen-Fuchs nodules.P" However, the fol lowing are more common in ocular sarcoidosis: intense vitritis with "snow balls;" extensive retinal involvement, including macular edema, pe riphlebitis, and subretinal neovascularization; and optic nerve invol vement. 54,1l7 Furthermore, with sarcoidosis, characteristic pulmonary, skin, and joint involvement occurs.P"

In the nineteenth century, some believed that suppuration in the in jured eye protected against the development of SO. Thus "beneficent sup puration" was intentionally induced to prevent the disease. 1 However, the only substantiated-and presently practiced-preven tive measure for SO is enucleation of the injured eye before sensitization occurs. Thus, no known prophylactic measure can prevent SO that occurs as a surgical complication. The rule of thumb is to enucleate within 14 days of injury. The origin of this rule is unclear, and it does not invariably prevent SO, because onset of the disease has been reported as soon as 5 days after injury.s,49 However, one study indicates that if SO has not de veloped, enucleation within 2 weeks of injury significantly improves visual outcome. When this was done, final visual acuity was no less than 20/70 in 80% of 34 patients,us

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Is enucleation beneficial after development of SO? Some studies sug gest that enucleation within 2 weeks of the onset of SO is associated with fewer ahd milder llS recurrencesv'!" and improved visual outcome. ,119 Howeve~, evidence also suggests that enucleation does not improve visual outcome." Because of the lack of consensus that enucleation improves vi sual outcome, because SO is very rare, and because the injured eye may become the eye with better vision, a widely held principle is to try to save the injured eye if any potential for useful vision exists. 52,116,lls,119 Not all patients with SO require systemic treatment. Topical steroids and mydriatics are used to control anterior uveitis, when present, and sys temic treatment is used for posterior uveitis that threatens or impairs vi sion. 115 Corticosteroids are the mainstay systemic treatment. Prophylactic corticosteroid 2 therapy does not necessarily prevent the disease. ,120 How ever, corticosteroid therapy after onset of SO has been associated with long-term visual acuity of at least 20/60 in a majority of patients in multi ple studies. 8,60,119,121 A high starting dose of prednisone, varying from 0.5 to 2 mg/kg/ day depending on the severity of the inflammation, usually is used. 52,115,116 As long as inflammation remains controlled, the initial dose can be tapered gradually by approximately 5 mg/week to a maintenance dose of 5 to 10 mg/ day (in adults) for several months. 115 However, fulmi nate disease may require intravenous pulse therapy. 52 Possible side effects must be considered before starting any treatment and patients must be monitored for them throughout treatment. For prednisone, they include secondary glaucoma, cataract formation, dia betes, systemic hypertension, myopathy, osteoporosis, peptic ulcer, psy chosis, and growth retardation (in children) .122 Cyclosporine (CSA) is a second-line treatment. Besides being used when the disease is poorly responsive to steroids or when steroids are ab solutely contraindicated, CSA is used in steroid responders and in patients who require a high maintenance dose of steroid to remain in remission (> 20-25 mg/day). Of all patients treated for SO at a uveitis clinic (32 pa tients), 22% (7 patients) were treated with CSA for one of the foregoing reasons. 10 CSA is useful for treating SO because it is a potent inhibitor ofT lymphocyte function, which plays an important role in the disease process. CSA is useful both for treating the disease itself and for inducing resolution of secondary choroidal neovascularization.l'" Three to 5 mg/kg/ day with 15 to 20 mg/ day of prednisone has been recommended.i'" Because of CSA's nephro- and hepatotoxicities, 122 renal and liver function, including 24-hour urine creatinine clearance and blood pressure, should be monitored. The cytotoxic agents azathioprine, methotrexate, chlorambucil, and cyclophosphamide are alternative second-line treatments. Bone marrow depression 122 is among the most common adverse reactions to all these agents. Potential side effects of chlorambucil and cyclophosphamide also include sterility and neoplasia, respectively.F'' The cytotoxic agents have been used successfully, often i'n combination with low-dose prednisone. 10, 121, 12'1~12(i

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The immunosuppressant FK506 (tacrolimus), which has mechanism of action similarcil was added if disease was severe.?' The most recent 1study reporting vi to that of CSA,54,26 was effective treatment for case of sual SO.127~tential adverse effectsSO included 32 patients followed for no more than 13 years tion,outcome data for include hypomagnesemia, renal dysfunc (mean, 5.6 neurological symptorns.l'" gIucose intolerance, and years) and found visual acuity of at least 20/40 in 16 (50%) and less than 20/200 in 10 (31 %). All patients except the efficacy of any Three months is a reasonable period to evaluate one received corticosteroids alone or combined with CSA or cyclophos phamide.!" treatment approach. 52,116 Usually, clinical parameters, including fluores cein angiography findings, are used to evaluate disease activity and thus treatment efficacy. However, the degree of secondary hypero~ia,66 serum beta-2 microglobulin levels/ 28 and serum sialic acid level! 9 might be useful adjuncts in this regard. Summary Short-term therapy with corticosteroids or other immunosuppressants has been recommended for surgical treatmentisof fearful postoperative complication because of Although uncommon, SO a ocular sequelae of SO (e.g., cataract, glaucoma) 130 and probablyeyes. It can result not only from pen its potential to blind both is advisable for any ocular surgery etrating ocular performed on surgery but also from nonpenetrating ocular procedures. Thus, it is important to a patient with a history of SO, even if the history is remote and the disease is consider in For cataractwho has undergone ocular surgeryeyes,develops bilateral quiescent. any patient extraction in sympathiz ing and not only the status ofuveitis,eye at the becauseof the procedure but postoperative the particularly time prompt, suffi cient treatment is required to maximize management, visual outcome. It is also impor tant to note that the disease may present with a including immunosuppressant use, critically affects visual outcome.l'" spectrum of clinical find ings, none of which is pathognomonic. Thus, suspicion
is important for making the diagnosis. Treatment should address the T-cell-mediated nature of the disease. With appropriate treatment, visual acuity of no less than 20/60 is likely. Prognosis However, before the start of treatment, which consists of immunosup pressants, infection must be ruled out and potential side effects of treat ments must be Early and sufficient treatment plays a major role in a history of SO A visual outcome. needs ample considered. Furthermore, any patient with retrospective study of 77 cases demonstrated a significant correlation be tween immunosuppressant coverage for ocular procedures. severity of inflammation in the exciting eye and visualthe disease may lead to safer acuity in the Better understanding of the pathogenesis of sympathizing treatments athat result in 3 months' visual outcome 9 cases cure. Mean eye after minimum of improved follow-up. All and a with while, severe (4+) inflammation inrelapsing nature, SO requires continual, of no more because of its the exciting eye had a visual outcome close surveillance, even than 20/70, whereas 14 years of quiescence. mild (1 +) inflammation retained after many of 815 patients with

vision of at least 20/70. In another retrospective study of 32 cases, visual outcome of no less than 20/40 (16 patients) was associated with early and aggressive treatment, whereas visual outcome of no more than 20/200 (10 patients) was associated with inadequate treatment re sulting in persisten t References inflammation (6 patients), macular scarring (2 pa tients), and secondary glaucoma (2 patients)."? 2. Albert DM, Diaz-Rohena R. A historical review of sympathetic ophthalmia and ill Because of the relapsing nature ofOphthalmol I 9RCJ;,)l: 1-14 follow-up is SO, close, long-term epidemiology. Surv required, even in 3.patients who Perkins ES. Sympathetic ophthalmitis, In: Duke-Elder S, ed. Diseases Duke-Elder S, have been sign-and-symptom-free for years. 2,42 With appropriate uveal tract. St and follow-up, studies indicate that of the treatment Louis: Mosby, 1966:558-593 4. visual acuity of at least Woods Ae. Sympathetic ophthalmia. AmJ Ophthalmol 1936;19:9-15 20/60 is not uncommon. Visual acuity was at least 5. Straub W. The first German to 23 years and treated with 20/60 in 9 of 17 patients (53%) followed 3 textbook of ophthalmology: "Augendienst" by G. Bartisch, corticosteroids.P" Another study1583. Doc OphthalmoI1988;68:105-114 20/60 in 14 of found visual acuity of 20/20 to 6. Fuchs E. Uber sympathisiercnde entzundung zuerst bemerkungeen uber serose trau 18 patients (78%) followed 7 monthsGraefes Arch Clin Exp OphthalmoI1905;6l:365~456 to 36 years (mean, 7.2 years). Treatment matische iritis. was corticosteroids,7.CSA, or R. Historische notizen uber or inBraille und die blindenschrift.An Monatsbl nation.P" Klin Kaden azathioprine, alone Louis combi additional study revealed visual acuity of no less than 20/50 in 14 of 20 Augenheilkd 1977;170:154-158 8. patients (70%) followedWinterno more thanuveitis: a clinical and pathologic study of the visual field. Am for Fe. Sympathetic 13 years (mean, 2.5 years). All J Ophthalmol 1955;39:340-347 patients received corticosteroids, and chlorambu9.

Lubin JR, Albert DM, Weinstein M. Sixty-five, years of sympathetic ophthalmia: a clinicopathologic review of cases (1~) 1 ')-1 97R). Ophthalmology I ~)80;R7: I 09-121