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10.7 Non-infectious Choroiditis andRetinitis

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adjuvants. Without adjuvants, injecting soluble retinal antigens fails to produce uveitis. The potential antigens include retinal-S antigen, interphotoreceptor-binding protein, recoverin, and melanin. Immunization with all these antigens has led to the development of autoimmune uveitis in animal models. Melanin proteins have been used to create a rat model of CD4+ T-cell- driven experimental autoimmune uveitis that mimics the pathology of SO [250].

The retinal-S antigen has been the most potential antigen studied of all the putative antigens, but its antibodies have not been detected in the sera of all SO patients [251].

Pathology ofSympathetic Ophthalmia

The pathology of SO was rst described by Dalen and later by Fuchs as nodular aggregates beneath the RPE layer and essentially consist of macrophages. In the late stages, the macrophages may be accompanied by degenerated RPE cells and a few lymphocytes. However, these nodules are present only in one-third of the pathology samples of SO [251]. The choroid is thickened and inltrated with lymphoid cells, epithelioid cells, and multinucleated giant cells. The iris likewise shows nodular inltration with lymphoid cells, multinucleated giant cells, and epithelioid cells. The nodular collection of epithelioid cells under the RPE corresponds to the points of leakage on FFA from the RPE.On electron microscopy, the separation of tight junctions of RPE over the Dalen Fuchs nodules has also been seen [252]. In both sympathetic ophthalmia and VKH, despite heavy inltration of the choroid with inammatory cells, RPE and choriocapillaris are preserved. It was suggested that the RPE might modulate inammation in these conditions and preserve the retina [253].

The mechanism of vision loss in SO remained unexplained as the retina is not primarily involved in SO. However, immune co-localization of TNF-α and its receptor inducible nitric synthase (iNOS) and the oxidative products nitrotyrosine have been localized to the photoreceptors of SO eyes explaining the apoptosis and photoreceptor cell death following oxidative stress in SO [254].

Clinical Picture ofSympathetic Ophthalmia

All patients who suffer from penetrating trauma should be counselled on reporting any symptoms in the contralateral eye for the early detection of SO. For several generations, SO has been described in the textbooks as a bilateral granulomatous pan uveitis that presents with mutton fat keratic precipitates, inammatory cells in the anterior chamber, or the vitreous cavity has been misleading. Yellow-white lesions may be seen in the retinal periphery if ocular media permits. There may be papillitis, optic atrophy, retinal vasculitis, and retinal detachment. This description ts in with the stage of chronic recurrent uveitis. This description has led to ignoring the earliest presentation of the SO in the earliest stages, i.e. the acute uveitic stage.

Early Symptoms ofSympathetic Ophthalmia

The earliest symptoms in the sympathizing eye may be mild pain, blurred vision, and loss of accommodation. The signs include optic disc oedema, yellow-white discrete lesions deep to the retina, and multifocal serous retinal detachment (Fig.10.21) [255].

In our tertiary care centre, we saw 40 patients with SO from 1989 to 2004, 75% of whom followed trauma and 25% followed surgery. Except for four cases, all presented in the acute stage of the disease. More than 50% of the sympathizing eyes presented only with posterior segment signs and had no anterior segment inammation. There was mild vitreous inammation in 75%, exudative retinal detachment in 73%, yellow-white peripheral lesions in 35%, optic disc oedema in 37%, and peripapillary CNV in 5% of the sympathizing eyes. All four patients who presented with a chronic stage of SO had sunset glow fundus and discrete white scars in the retina. FFA ndings were similar to that seen in the VKH disease and were noted in 85% of the eyes. These consisted of delayed choroidal lling, pinpoint hyperuorescence, and late pooling of the dye (Fig.10.21). All 15 eyes that showed optic disc oedema showed optic disc staining on FFA. On ultrasonography,

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10 Retinal andChoroidal Infections andInammation

Fig. 10.21 (a–g): A 24-year-old man reported sustaining an open globe zone II injury in the right eye 2days after hammering a chisel (a). Visual acuity was light perception in the right eye and 6/6in the left eye. He underwent a primary repair. Twenty days later, he returned with multifocal retinal detachments in the left eye without any inammatory reaction (b). FFA showed an initial hypo-

uorescent pinpoint lesions which became hyperuorescent and pooled dye in late frames (c–e). USG showed choroidal thickening (f) and OCT showed subretinal uid with septa (g). He was treated with intravenous methylprednisolone followed by oral corticosteroids. (h–k) A week later, his retinal detachment had resolved (g, h). Nine-month follow-up mild pigmentary changes (i, j)

10.7 Non-infectious Choroiditis andRetinitis

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63% of the eyes (12 of the 19 eyes) showed diffuse thickening of the choroid. The OCT was done in 10 eyes, and in all, it showed serous retinal detachment. Ten eyes were enucleated for histopathology, and all showed granulomatous inltration of the choroid, with eosinophilic inltration in four eyes and retinal perivascular inltrates in one eye. The patients were treated with aggressive corticosteroid therapy and immunomodulatory therapy. Seventy- three percent of the eyes achieved nal visual acuity of 6/12 or better in a median followup of 5years. Thirty percent of the sympathizing eyes showed a severe granulomatous anterior uveitis recurrence on corticosteroid tapering. Notably, 5% of the eyes showed posterior segment recurrence in the form of exudative retinal detachment [256].

Similarity ofSympathetic Ophthalmia andtheAcute Uveitic Stage ofVKH Disease

The clinical picture of the acute stage of SO and the acute uveitic stage of the VKH disease are similar. The FFA in patients with SO is identical to those with VKH disease. The FFA is characterized by focal delayed choroidal lling and multifocal pinpoint dye leakage with late dye pooling in VKH disease and SO. Several cases of SO have been described in the past that showed similarity between the clinical features (vitiligo, poliosis, dysacusis, and meningitis-like symptoms) between the SO and the VKH disease [117, 118, 257]. The exciting eye was enucleated and subjected to histopathology in four SO patients who developed vitiligo, poliosis, dysacusis, and/or meningitis mimicking complete VKH disease. All the eyes revealed histopathological features of granulomatous choroiditis with chorioretinal adhesions and pigment migration into the retina and features also seen in the VKH eyes [258]. The only differentiating feature of SO from VKH is the history of penetrating trauma in the former.

Enucleation oftheInjured Eye toPrevent Sympathetic Ophthalmia Is aMyth

The eye that undergoes trauma or surgery is termed the exciting eye, and the contralateral eye that develops granulomatous inammation is termed the sympathizing eye. Both eyes show similar granulomatous pathology, except the injured eye

also shows changes resulting from trauma. While nearly 50% of the eyes who have developed SO do so within 2weeks to 3months of injury, more than 90% of SO develop it in the rst year. The rule of thumb is no longer valid, with little evidence that SO can be prevented in the contralateral eye if the traumatized eye is removed within 2weeks. The SO may still happen despite the enucleation of the inciting eye [259]. The shortest interval between the traumatic event and the onset of SO has been 5days [260]. Not only does the removal of the eye not exclude the risk of SO, but with the current surgical techniques, it is possible to put together even the badly injured eyes.

Moreover, even if the SO develops, powerful therapeutic drugs are now available to control and limit the damage in the sympathizing eye. If the injured eye is badly mutilated and the surgeon feels that anatomical integrity cannot be restored, then instead of enucleation with its psychological trauma and phantom pain, it should be eviscerated to allow for the implantation of a movable prosthesis [259]. Evisceration does not appear to increase the risk of SO.In one large series, not a single case of SO developed following evisceration of the 491 traumatized eyes [261].

10.7.3 Organ-Specic (Ocular)

Immune-Mediated Disorders

Widely known as ‘white dot syndrome’, this is a group of disorders characterized by discreet white lesions deep in the retina, often bilateral, and often seen in young to middle-aged women. The salient clinical and imaging features of each of these disorders are given in Box 10.11. There is no anterior segment inammation, although some have mild vitreous inammation. Most of them cause photopsia or blurring of vision and scotomas. The availability of multimedia imaging tools has made it possible to differentiate them. The pathogenesis is unknown, but there is evidence of primary choriocapillaris involvement and loss of outer retinal microstructures. Differential diagnoses in the white dot syndromes include sarcoidosis, TB, syphilis, and primary vitreoretinal lymphoma, which may have clinical presentation indistinguishable from these syndromes and need to be

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Box 10.11 Organ-Specic (Ocular) Immune- Mediated Inammations

Disorder Clinical characteristics Imaging studies MEWDS

1. Young women > men

2. Photopsia, blurring of vision

3. Unilateral

4. Optic disc oedema

5. Macular granularity

6. Multifocal white lesions in paramacular and peripheral fundus

7. Spontaneous resolution in ~8weeks

FFA:

1. Hyperuorescent dots (<100μ), in wreath conguration

2. OD staining

3. Minimum staining of white dots

ICG: Hypouorescent dots (>200μ) in late frames FAF: Hyperautouorescent OCT: Hyperreective lesions cantered on the

ellipsoid zone protruding from RPE into outer nuclear layer OCTA: Flow voids in CC All changes reversible on healing

APMPPE

1. Young, preceding u

2. Sudden loss of vision, photopsia, scotomas

3. Sequential bilateral creamy placoid lesions in outer retina

4. Lesions heal spontaneously with pigmentary changes

FFA: Initial hypouorescent, late hyperuorescence

ICG: Hypouorescent throughout FAF: Hypoautouorescent with a ring of

hyperautouorescence OCT: Hyperreective material in the outer retina, disruption of EZ and IZ; SRF+ OCTA: Flow void in CC All changes reversible on healing except transmission defects on FFA

PIC

1. Young, myopic women

2. Blurring, photopsia, metamorphopsia

3. Discrete, 100-300μ multifocal outer retina and inner choroidal lesions in macula, heal with punched-out atrophic scars

4. Subfoveal haemorrhage

5. Serous macular RD

FFA: Hyperuorescence in early and late frames; Type 2 CNV hyperuorescence in macula

ICG: Hypouorescent lesion throughout FAF: Hyperautouorescence OCT: Hyperreective lesions in inner choroid

with conical RPE elevation, with intact BM, photoreceptors not visible in active lesions OCTA: CNV between RPE and neurosensory retina

IMFC

(MFC

with panuveitis)

1. Young myopic women

2. Photopsia, scotomas

3. Unilateral/bilateral/sequential

4. Multifocal choroiditis lesions or scars

5. Vitreous cells

6. Recurrent, progressive

7. CNV

FFA: Non-contributory in acute stage. Some hyperautouorescence in late frames. Transmission defects in scars. Type 2 CNV ICG: Hypolesions from 50 to 400μ, most remain hypouorescent in late frames

FAF: Hyperautouorescence OCT: Hyperreective material in the inner choroid

elevating the RPE, with a rupture at the peak of BM/RPE and material extending into outer retina. Disruption of EZ, IZ, and ELM increased light transmission through the lesion OCTA: CC ow voids reversible in smaller lesions

d, e

AZOOR

1. Young to middle-aged healthy women

2. Moving photopsia-lightening in a thunderstorm, photophobia, scotoma, blind spot in temp eld, visual eld loss, night vision problems

3. Bilateral asymmetric disease

4. Peripapillary normal or subtle lesion, white demarcation line between normal and affected retina may be prominent but transient; trizonal lesions are diagnostic

FFA: Non-contributory in acute, window defect in late stage

ICG: Non-contributory in acute, trizonal pattern FAF: Patch hyperautouorescence, progressive,

later hypoautouorescence, hyperautouorescent demarcation line; normal outside the demarcation line OCT: Loss of EZ, thickening of outer plexiform layer and loss of outer nuclear layer; foveal centre may be spared for a long time loss of RPE in late stages

5. Bone specule pigment and atrophy

10.8 Multiple Evanescent White Dot Syndrome (MEWDS)

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Disorder Clinical characteristics Imaging studies

f, g

BCR

AMN

h,i

1. Middle-aged, F>M, Caucasians

2. HLA-A29*02in >95%

3. Blurring of vision or oaters both eyes

4. Creamy oval/streak lesions choroidal 500–1500μ radial to optic disc

5. Vitritis

6. CME

7. Retinal vasculitis

8. ODE

9. Cellophane maculopathy

1. Young women

2. Unilateral or bilateral Paracentral scotomas after u-like illness, transient or permanent

3. Fundus shows multiple reddish brown, sharp petaloid lesions deep in the retina centred around foveal centre

4. >100μ outer retinal changes are often permanent

FFA: delayed A-V transit; hypolesions in the early and mild hyperuorescence in late frames; late OD staining; CME, retinal perivenous staining and leakage ICG: Most sensitive tool, hypouorescent lesions corresponding to creamy lesions aligned with choroidal vessels. FAF: Linear hypoautouorescence along retinal vessels OCT: Disruption of ellipsoid zone, focal to generalized; outer retinal atrophy ERG: Full eld and mfERG shows delayed implicit time and decreased amplitude

NIR imaging: Shows hyporeective sharply dened lesions in the macula

FFA: Normal ICG: Normal FAF: Normal OCT: Loss of ellipsoid zone/IZ and thinning of

outer nuclear layer and OPL hyperreectivity OCTA: Flow decit in deep capillary plexiform layer. Flow may reverse but OCT changes may not revert VF: Paracentral scotoma

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MEWDS multiple evanescent white dot syndrome, FFA fundus uorescein angiography, ICG indocyanine angsiography, FA F fundus autouorescence, OCT optical coherence tomography, OCTA optical coherence tomography angiography, OD optic disc, CC choriocapillaris, PIC punctate inner choroidopathy, RD retinal detachment, CNV choroidal neovascular membrane, IMFC idiopathic multifocal choroidopathy, RPE retinal pigment epithelium, BM Bruch’s membrane, EZ ellipsoid zone, IZ interdigitating zone, ELM exter-

excluded. Except for MFC and AZOOR, which require corticosteroids and immunosuppressive therapy, most white dot syndromes resolve spontaneously with or without residual changes.

10.8 Multiple Evanescent White Dot Syndrome (MEWDS)

Multiple evanescent white dot syndrome (MEWDS) is a rare disorder usually seen in young myopic women who present with photop-

nal limiting membrane, AZOOR acute zonal occult outer retinopathy, BCR birdshot chorioretinopathy, ERG electroretinography, mfERG multifocal ERG, AMN acute macular neuroretinitis, NIR near infrared, OPL outer plexiform layer

References

Marsiglia etal. [262]; b Testi etal. [263]; c Ahnood et al. [264]; d Pichi et al. [202]; e Mrejen et al. [265]; f Minos et al. [266]; g Fogel-Levin etal. [267];

Yzer etal. [268]; i

Fawzi etal. [269]

sia and blurring vision (Fig.10.22). The fundus examination reveals unilateral optic disc oedema and multiple white lesions in the paramacular and retinal periphery. The FAF imaging is highly diagnostic of MEWDS (Fig. 10.23). Most of these white dot syndromes have hyperautouorescence due to exposure of the pigments in the RPE layer due to loss of the overlying photoreceptors and their pigments, which normally block the autouorescence signals from the RPE [267]. Changes are reversible to a large extent in MEWDS (Fig.10.23g).

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Fig. 10.22 A 39-year-old man presented with oaters in left eye for one week, with history of viral fever a few months ago. His visual acuity was 6/6/ in both eyes. Visual eld testing revealed enlargement of blind spot (red

Fig. 10.23 Same patient with MEWDS as in Fig.10.22, showing fundus photographs (a, b). Fluorescein angiography shows wreath-like pattern (blue arrows) (c, d). Fundus autouorescence shows normal right eye (e) and characteristic hyperautouorescent changes in left (f) eye.

arrow) in left eye (a). Right eye was normal (b). Imaging revealed a diagnosis of MEWDS. (Images courtesy of Dr. Padmamalini Mahendradas, Uveitis and Ocular Oncology, Narayana Nethralya, Bangalore, India)

Follow-up at 6months reveals near complete recovery of autouorescence ndings (g). (Images courtesy of Dr. Padmamalini Mahendradas, Uveitis and Ocular Oncology, Narayana Nethralya, Bangalore, India)

10.9 Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

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10.9 Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is characterized by the

sudden onset of vision loss in young women preceded by a u-like illness. It is usually bilateral, but the other eye may have sequential involvement within a few days of the onset. The fundus examination reveals multifocal creamy white placoid lesions in the outer retina (Fig. 10.24).

Fig. 10.24 Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) in a 24-year-old man who had viral fever 8days ago. There are asymmetric bilateral choroiditis lesions, with right eye (a) affected less than left eye (b). FFA shows hypouorescent lesions in early phase

(c), which become hyperuorescent in late phase (d). A few weeks later, the choroiditis lesions resolved completely (e, f). (Images courtesy of Dr. Padmamalini Mahendradas, Uveitis and Ocular Oncology, Narayana Nethralya, Bangalore, India)

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The lesions heal by restoring the photoreceptors’ integrity and return of vision [262, 263, 270]. Many inammatory diseases, autoimmune vasculitis, infections, and vaccines have been reported preceding the onset of APPMPPE [271]. A signicantly higher frequency of HLA-B7, a class I antigen, and HLA-DR2, a class II antigen, has been reported in APMPPE patients with a relative risk of 3.38 and 3.34, respectively, lending support to a suggestion that this disorder may be caused by underlying immune mechanisms [272].

10.10 Punctate Inner Choroidopathy andIdiopathic Multifocal Choroidopathy (PIC andIMFC)

Most experts believe that punctate inner choroidopathy (PIC) and idiopathic multifocal choroiditis (IMFC) represent a spectrum of diseases. Idiopathic multifocal choroidopathy has been named in the past with various eponyms, including pseudo-presumed ocular histoplasmosis syndrome, multifocal choroiditis with panuveitis, and multifocal inner choroidopathy. Both of these disorders get complicated by the development of choroidal neovascular membranes (CNV) [202, 264]. The acute lesions of IMFC and PIC get picked up by the FAF imaging.

10.11 Acute Zonal Occult Outer Retinopathy (AZOOR)

The symptoms of moving photopsia, ‘lightning strike in a thunderstorm’, are highly suggestive of acute zonal occult outer retinopathy (AZOOR). They should prompt fundus autouorescence studies as the fundus in the initial stages may look normal. A trizonal pattern of autouorescence is highly characteristic of AZOOR [265]. Late stages of AZOOR result in retinal atrophy,

bone-corpuscle pigmentation in the affected quadrants, and optic atrophy. These need to be differentiated from autoimmune retinopathies, retinal degenerations, and dystrophies like retinitis pigmentosa and optic neuropathies [265].

10.12 Birdshot Chorioretinopathy (BCR)

Birdshot chorioretinopathy (BCR) is strongly associated with HLA-A29*02in Caucasians and rarely if ever, seen in Asians or Blacks. The diagnosis of BCR is often delayed due to very subtle clinical lesions that may be missed in a routine examination and need a high index of suspicion for making an early diagnosis. Patients are highly symptomatic even in the presence of normal or near-normal vision. It is a chronic recurrent inammatory disease and needs immunosuppressive therapy to prevent retinal atrophy and optic atrophy [266, 267].

10.13 Acute Macular Neuroretinitis (AMN)

Acute macular neuroretinitis (AMN) is rare and often seen in young to middle-aged women. It often follows a u-like illness or even a sudden hypotension attack may precipitate this disorder. While the fundus lesions may be very subtle, near-infrared imaging shows hyporeective changes centred around the fovea. There are two types of AMN, type 1, also termed paracentral acute middle maculopathy (PAMM) due to occlusion of the deep capillary plexus and results in hyperreectivity of the inner nuclear zone and the outer plexiform layer and type 2, which is characterized by the loss of outer nuclear layer and hyperreectivity of the outer plexiform layer. Optical coherence tomography angiography shows ow voids in the deep retinal capillary plexus [273, 274]. The PAMM or AMN lesions may follow sickle cell disease [275].

References

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