2. Inflammatory Chorioretinopathies of Unknown Etiology
white dot syndromes

3. a group of idiopathic multifocal inflammatory conditions involving the retina and the choroid

4. acute posterior multifocal placoid pigment epitheliopathy (APMPPE)
birdshot chorioretinopathy
multiple evanescent white dot syndrome (MEWDS)
multifocal choroiditis with panuveitis (MFC)
serpiginous choroiditis

5. Discrete, multiple, well-circumscribed yellow-
white lesions at the level of the retina, outer retina, RPE, choriocapillaris, and choroid

6. The etiology of the white dot syndromes is unknown

7. Bilateral involvement ( MEWDS)
younger than 50 years of age
(birdshot retinochoroidopathy and serpiginous)

8. Common presenting symptoms:
Photopsias
Blurred vision
Nyctalopia
Floaters
Visual field loss (blind spot enlargement )
Mild vitritis ( usually)

9. differential diagnosis :
Syphilis
Diffuse unilateral subacute neuroretinitis (DUSN)
Tuberculosis
Toxoplasmosis
Pneumocystis choroidopathy
Candidiasis
Acute retinal necrosis (ARN)

10. Ocular histoplasmosis syndrome (OHS)
Sarcoidosis
Sympathetic ophthalmia
VKH syndrome
Intraocular lymphoma

11. Morphology
Evolution
Distinct natural histories
Angiographic behavior

12. a prodromal viral syndrome can be identified

13. Acute posterior multifocal placoid pigment epitheliopathy (APMPPE)

14. Healthy young adults
Typically surrounding an influenza-like illness (50%)
Men and women being affected equally
Usually nonrecutrent disease

15. A sudden onset of bilateral
Asymmetric visual loss associated with central and paracentral scotoma

16. Minimal anterior segment inflammation
Mild to moderate vitritis

17. Funduscopic findings:
multiple, large, flat, yellow-white placoid lesions at the level of the RPE, varying in size from 1 to 2 disc areas, located throughout the posterior pole to the equator

18. CME is uncommon

19. The lesions resolve over a period of 2 to 6 weeks
leaving a permanent geographic-shaped alteration in the RPE

20. The diagnosis of APMPPE is based on the characteristic clinical presentation and characteristic FA findings during the acute phase of the disease

21. fluorescein angiography:
Early hypofluorescenc
Staining in the late phase

24. Serpiginous choroidopathy

25. Uncommon
Chronic, progressive inflammatory
Adult men and women equally
Second to sixth decades of age life
Minimal vitreous involvement
A quiet anterior chamber

26. Gray-white lesions at the level of the RPE projecting in a pseudopodial or geographic manner from the optic nerve in the posterior fundus

27. Acute lesions are commonly located adjacent to atrophic scars

28. The disease course is marked by progressive centrifugal extension, with marked asymmetry between the 2 eyes

29. Fluorescein angiography :
Early hypofluorescence of the active lesions
Staining of the active edge of the lesion in the later stage

30. Systemic immunomodulation has been suggested as first-line therapy because
corticosteroids alone are ineffective

33. Multiple evanescent white dot syndrome (MEWDS)

34. Unilateral (80%)
Central or peripheral scotoma
Healthy young (10-47 years)
Moderately myopic females (90%)
Frequently surrounding a flulike prodrome

35. multiple, discrete white orangish spots( μm) at the level of the RPE or deep retina, typically in a perifoveal location

36. These spots are transitory and are frequently missed; they leave instead a granular macular pigmentary change

37. Few associated vitreous cells
Mild blurring of the optic disc

38. Punctate hyperfluorescent lesions in a wreathlike configuration surrounding the fovea that stain late

39. The prognosis is excellent, and vision is completely recovered in 2-10 weeks without treatment

42. Birdshot retinochoroidopathy

43. Females (common)
The fourth decade of life
HLA-A29 (80%-98%)

44. Anterior segment inflammation may be minimal or lacking
Varying degrees of vitritis ( commonly)

45. Multifocal,hypopigmented, ovoid, cream-colored lesions ( μm) at the level of the choroid and RPE in the postequatorial fundus

46. These lesions radiate from the optic nerve and follow the larger choroidal vessels

47. Retinal vasculitis
CME
Optic nerve head inflammation

48. Fluorescein angiography :
Mild hyperfluorescence and staining in the late phase
Identifying active retinal vasculitis, CME, and optic nerve head leakage

52. The course is generally marked by multiple exacerbarions and remissions

53. Treatment: Systemic corticosteroids
Corticosteroid-spadng immunomodulatory agents
Periocular corticosteroid injections

54. Conclusion:
Because of the significant overlap among them, the various white dot syndromes may just represent a spectrum of the same disease