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REVIEW Retinal Insider Table 1. Clinical & Angiographic Characteristics of Placoid White Spot Syndromes Lesion characteristics Presenting symptoms Gender, Age Laterality FA characteristics ICG characteristics OCT fi ndings FAF fi ndings Complications Treatments Systemic associations Course APMPPE Multiple posterior, creamy white-yellow lesions of varying sizes; fade in two to three weeks with subsequent RPE mottling. Sudden vision loss, photopsias, scotomas. M = F, young Bilateral, usually symmetric Early hypofl uorescence followed by late staining. Hypofl uorescence throughout, less defi ned in late phase. Acute: Dome-shaped elevations of the EZ band, hyperrefl ective material, subretinal fl uid. Late: EZ thickening, ONL thinning, RPE thickening. Resolution: reconstitution of the EZ band, minimal RPE changes. Acute lesions demonstrate hypoautofl uorescence and develop hyperautofl ourescence with resolution. Rarely signifi cant RPE and photoreceptor atrophy or CNV resulting in vision loss. Generally none, occasionally corticosteroids. Serpiginous Choroiditis Classically, serpentine gray or yellow peripapillary placoid lesions. In the macular variant, there is no extension to the disc. Loss of vision, scotomas, metamorphopsia Slightly more common in males, young to middle age Bilateral. Usually one eye is active at a time. Early hypofl uorescence followed by progressive hyperfl uoresence at lesion margins with late staining. Hypofl uorescence throughout, less pronounced in late phase Acute: Hyperrefl ectivity of outer retina and RPE Resolution: Loss of the RPE, photoreceptor outer segments, and EZ band; normal ONL; choroidal hyperrefl ectivity. Active lesions: Hyperautofl uorescent Inactive lesions: Hypoautofl uorescent Transitional stage: Hypoautofl uorescent halo surrounding edges of active hyperautofl uorescent lesion. CNV and CME in up to 20%. PED, BRVO also reported. Corticosteroids, plus other immunosuppressants, reservedly alkylating agents. Viral prodrome, CNS signs. Increased prevalence of systemic autoimmunity; reports of HLA-B27, Crohn’s disease, celiac disease, and also sarcoid. Acute decrease in vision with spontaneous recovery and good fi nal visual acuity. Relapsing and progressive nature, often with loss of central vision in at least one eye. Relentless Placoid Chorioretinitis Small (≤1/2 disc area), creamy white placoid lesions at the level of the RPE, anterior and posterior to the equator. Pigmented atrophy may result within weeks, or lesions may persist and grow with new lesions developing over time. May end up with hundreds of lesions. Decreased vision, fl oaters, metamorphopsia Possible male preponderance, young to middle age Typically bilateral (80%) Early hypofl uorescence followed by late staining. Hypofl uorescence throughout Acute: Hyperrefl ectivity of the inner and outer retinal layers, subretinal fl uid. Resolution: Normal anatomy reestablished. (time-domain OCT fi ndings) Extensive confl uent areas of marked hypoautofl uorescence corresponding to areas of chorioretinal atrophy. Subretinal fi brosis, ERM, subretinal fl uid reported. Prolonged corticosteroids; addition of other immunosuppressants also reported. Hashimoto thyroiditis, aseptic meningitis, type 1 diabetes mellitus reported. Acute loss of vision with progression and recurrence and growth of new lesions over months to years. Good fi nal acuity if no foveal involvement. Persistent Placoid Maculopathy Geographic central whitish plaques at the level of the RPE, centered around the fovea, not contiguous with the optic disc. Lesions persist for months to years but become fainter with time. Mild decrease in vision unless CNV present, photopsias, dyschromatopsia Possible male preponderance (only eight cases), older age (>50 yrs) Bilateral, symmetric Early hypofl uorescence with late partial fi lling; no marked leakage or staining. Hypofl uorescence throughout Acute: Retinal thinning with photoreceptor and RPE disruption Stability: Well-defi ned areas of photoreceptor loss, collapse of the outer plexiform layer and thinning of the chorio capillaris. Speckled pattern of hyper- and hypoautofl uorescence in the macula. High risk for CNV with disciform scar formation, rare signifi cant RPE atrophy. Oral and periocular corticosteroids; addition of other immunosuppressants such as cyclosporine. None Persistent lesions with mild decrease in visual acuity and high risk of CNV development, potentially resulting in loss of central vision. 46 | Review of Ophthalmology | February 2014
However, this subset of patients responded to increased oral corticosteroids or the addition of immunosuppressive therapy, supporting the former hypothesis. Thus, identifying the tubercular variant of serpiginous choroiditis is critical for initiation of appropriate antibiotics in combination with oral steroid therapy and one should not terminate antitubercular treatment even in the setting of initial paradoxical worsening. Relentless Placoid Chorioretinitis Relentless placoid chorioretinitis (RPC) is an entity that has features resembling both APMPPE and serpiginous choroiditis, but with an atypical retinal distribution and clinical time course. 27 The hallmark of this disease is the development of numerous new lesions during the disease course, which may span up to two years, eventually resulting in 50 to hundreds of lesions. Peripheral lesions can precede or occur simultaneously with posterior involvement and recurrences do not necessarily initiate at the edges of prior lesions (as in serpiginous). Because of its shared features with APMPPE and serpiginous choroiditis, this entity was termed “ampiginous” by Robert B. Nussenblatt, MD. 9,28 RPC presents in young patients, usually with a sudden decrease in vision and/or metamorphopsia with no history of a viral prodrome. An anterior chamber reaction or vitritis may be present. 14,29 Patients exhibit small, white, placoid lesions at the level of the RPE both anterior and posterior to the equator. Some of these lesions develop pigmented chorioretinal atrophy within weeks while others have a drawn out course of persistent activity or new growth. Angiographic findings are similar to those of APMPPE and serpiginous choroidopathy. 27,28,30 Only one case of RPC with OCT imaging 31 and a different case with FAF imaging 16 have been reported. On time-domain OCT, the active stage of the disease demonstrated hyperreflectivity of the inner and outer retinal layers with subfoveal fluid accumulation and a pigment epithelial detachment. With quiescence, normal foveal anatomy was reestablished. 31 FAF revealed extensive confluent areas of marked hypoautofluorescence corresponding to areas of chorioretinal atrophy. 16 Vision can decrease significantly in RPC, especially with foveal involvement. However, if treated with prolonged systemic corticosteroids, most patients can recover most of their prior vision. 27 In the absence of treatment with systemic steroids, final visual acuity tends to be compromised with prolongation of disease course. 28 Complications of RPC include CNV, subretinal fibrosis, subretinal fluid and epiretinal membrane formation. Persistent Placoid Maculopathy Persistent placoid maculopathy (PPM) was first described by Pamela Golchet, MD, and colleagues in 2006. 32,33 It resembles macular serpiginous choroiditis in its early involvement of the macula and predominantly affects middle-aged Caucasian males. Unlike in macular serpiginous choroiditis, patients with PPM initially present with only mild visual symptoms. Anterior chamber inflammation or vitritis is typically absent. 32,33 On ophthalmoscopy, jigsaw-pattern, whitish placoid lesions centered around the fovea that are not contiguous with the optic disc (See Figure 4A) are noted. Unlike serpiginous or macular serpiginous choroiditis, PPM lesions have a longer time course and gradually fade over months to years without the development of new lesions. FA demonstrates early hypofluorescent plaques that partially fill in late phases of the study (See Figures 4B and 4C). ICGA shows hypofluorescent plaques throughout the study (See Figure 4D). SD-OCT shows retinal thinning with photoreceptor and RPE disruption. Once the disease is stable, SD-OCT shows well-defined areas of photoreceptor loss, collapse of the outer plexiform layer and thinning of the choriocapillaris. 34 In the presence of CNV, intraretinal fl uid or neurosensory detachment may be present. 35 FAF shows a speckled pattern of hyper- and hypo-autofluorescence in the macula. 34 Despite macular involvement, visual acuity is only mildly affected in PPM, with good prognosis for visual recovery unless RPE atrophy or CNV develops. While development of RPE atrophy is rare, CNV occurs at a much higher incidence in PPM than any of the previously described placoid diseases (only three eyes of 16 total eyes reported thus far did not develop CNV). 32-34 Treatment with oral or periocular corticosteroids and cyclosporine have resulted in improvement in visual acuity prior to complications with CNV. 32-35 In one case, chronic immunosuppression was initiated early in the diagnosis of PPM and no CNV developed in either eye at one-year follow-up. 34 Treatment strategies for PPM-related CNV prior to the age of anti-VEGF agents have included sub-Tenon’s and intravitreal triamcinolone acetonide, oral prednisone, laser photocoagulation, photodynamic therapy and submacular surgery, with limited success and subsequent formation of disciform scarring in the majority of cases. 32,33 There is one reported case of PPMrelated CNV treated with intravitreal bevacizumab with good visual outcome followed over a period of two years. 35 A summary of the clinical and angiographic characteristics of the February 2014 | Revophth.com | 47
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