Common Symptoms
Typically presents with unilateral vision loss in fourth to seventh decades of life but usually have bilateral fundus findings as below; paracentral or central scotomas; decreased vision if lesions involve the fovea (75% of patients develop central loss of vision over the course of the disease in at least one eye). The recurrence of symptoms is common, usually months to years after the initial onset.
66.1.2 Exam Findings
Active Classic Variant
Yellow–gray peripapillary lesions with helicoid or serpentine appearance with centrifugal progression. Mild vitritis may be present (reported in 33% of cases).
Macular Variant
Lesions similar to the classic presentation; however, lesions initiate in the macula and therefore portend a poorer prognosis.
Inactive/Chronic
Geographic areas of chorioretinal atrophy, subretinal fibrosis, and retinal pigment epithelial clumping (▶ Fig. 66.1).
Fig. 66.1 Fundus photograph of inactive serpiginous choroiditis with geographic areas of atrophy in a helicoid pattern, retinal pigment epithelial clumping, and fibrosis.
Recurrence
New yellow placoid lesions at the edge of old atrophic scars (▶ Fig. 66.2).
Fig. 66.2 Fundus photograph demonstrating recurrent serpiginous choroiditis with activity at the fovea and inferior border of an area of chorioretinal atrophy.
Tuberculosis-Related Serpiginous Choroiditis
May present with vitritis and more peripheral lesions.
Other possible ocular findings include choroidal neovascularization (in up to 20% of patients), optic disc edema or neovascularization of the disc, retinal vasculitis (secondary to the extension from underlying inflammation), vascular occlusion (due to inflammation-related obstruction), and cystoid macular edema.
66.2 Key Diagnostic Tests and Findings
66.2.1 Optical Coherence Tomography
Outer retinal atrophy, loss of the inner segment/outer segment junction, and hyperreflectivity of underlying choroidal vasculature. Active lesions may demonstrate increased reflectivity in the outer retina.
66.2.2 Fluorescein Angiography or Ultra-Widefield Fluorescein Angiography
Active, Acute Phase
Early hypofluorescence due to choriocapillaris hypoperfusion and blocking from the edematous outer retina, with late staining of the lesion margins.
Chronic
Early hyperfluorescence from window defects secondary to retinal pigment epithelial atrophy or hypofluorescence from choriocapillaris nonperfusion, with late leakage adjacent to the margins secondary to choriocapillaris injury (▶ Fig. 66.3).
The choroidal neovascular membrane may be noted as late leakage noted from the margin of the lesion.
Fig. 66.3 (a) Arterial phase of fluorescein angiogram in serpiginous choroiditis, showing hypofluorescence of the atrophic areas due to choriocapillaris nonperfusion. (b) Late frame of fluorescein angiogram in serpiginous choroiditis, showing continued central hypofluorescence of the atrophic region with hyperfluorescence and staining of the lesion margins consistent with choriocapillaris injury.
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