1. Macular Invovement in Posterior Uveitis
بسم الله الرحمن الرحيم
Macular Invovement in Posterior Uveitis
F. Kianersi M.D 1386 / 8 / 3

2. Posterior Uveitis is one of the vision threatening diseases especially when the Macula is involved.
Several Posterior Uveitic entities involve the Macula, which can either be:
Infectious or
Non-Infectious.

3. Common Posterior Uveitic Entities Invoving Macula
Infective causes
Toxoplasmosis
b. Toxocariasis
c. Tuberculosis
d. Herpetic

4. Common Posterior Uveitic Entities Invoving Macula
Non-Infective Causes
Acute Posterior Multi Focal Placoid Pigment Epitheliopathy (AMPPE)
Multiple Evanescent White Dot Syndrome (MEWDS)
Macular Geographic Helicoid Peripapillary Choroidopathy
Birdshot Choroidopathy
Presumed Ocular Histoplasmosis Syndrome (POHS)
Retina Pigment Epithelitis (Krill's disease)
Punctate Inner Choroidopathy
Sub Retinal Fibrosis and Uveitis Syndrome
Harada's disease
Sympathetic Ophthalmia
Multifocal Choroiditis
Sarcoidosis
Behcet Disease.

5. TOXOPLASMOSIS

6. TOXOPLASMOSIS
It is the most common cause of Posterior Uveitis in the Immunocompetent patients.
Toxoplasmosis is caused by the obligate Intra-Cellular Protozoan Toxoplasma Gondii.

8. Most often is Congenital.
Toxoplasmic Retinochoroiditis is Unilateral in 72 to 83% of the cases.
Ocular Toxoplasmosis occurs from activation of cysts deposited in or near the Retina.

9. Congenital Toxoplasmosis
Most commonly acquired during the 3th Trimester of Pregnancy.
Infants are usually asymptomatic.

10. Peripheral Retinochoroidal scars are the most common ocular finding occurring in 82% of the patients.
However, Toxoplasma has a strong predilection for the Posterior Pole, particularly the Macular region.

11. Typical Congenital Toxoplasmic Retinochoroiditis Macular Cicatricial Lesion, consisting in:
Radial Deposition of Pigment around a Central Necrotic Zone.

12. Recurrent lesions frequently develop at the borders of the old Toxoplasma scars, so called Satellite lesions.

13. A Yellowish White or Grey Exudative lesion is seen with ill defined borders because of surrounding area of Retinal Edema.
Adjacent Choroiditis, Retinal Vasculitis, Hemorrhage and Vitritis may be seen.

14. An Active lesion accompanied by a severe Vitreous Inflammatory reaction will have the classic “Headlight in the Fog" appearance.

15. Healed Scar typically has well defined borders with Central Retinochoroidal Atrophy and peripheral RPE hyperplasia.

16. Healed Scar

17. Toxoplasmosis Neuroretinitis
Active lesions localized to the Juxtapapillary region, aggressively involving the Retina and Optic Nerve.

18. Toxoplasmosis Neuroretinitis
Papillitis with Disk Hemorrhages, Venous Engorgement and overlying Vitritis.

19. Toxoplasmosis Neuroretinitis
Later, a Juxtapapillary Retinochoroiditis and Macular Star develop.

20. Toxoplasmosis Neuroretinitis
Toxoplasma Neuroretinitis is an Ophthalmic Emergency and requires prompt treatment.

21. Complications of Ocular Toxoplasmosis
Secondary Glaucoma,
Cataract,
Vitreous Hemorrhage,
Retinal Detachment,
Choroidal Neovascular Membrane (CNV),
Cystoid Macular Edema (CME),
Ocular Vascular Occlusions,
Optic Atrophy.

22. Diagnosis
Diagnosis of ocular Toxoplasma is based mainly on clinical findings.
Serological studies are helpful in suspected cases or the ones with atypical presentation.

23. Treatment

24. Treatment
Despite recent advances, an ideal combination that destroys the Tissue Cysts and prevents recurrence has not been found.
Current therapies are targeted mainly at the Active disease.

25. A combination of the following drugs are used:
Pyrimethamine:
Loading dose: 100 mg (1st day), followed by 25 mg once daily.
Sulfadiazine:
4 Gr daily divided in every 6 hours.
For 4 to 6 weeks.
These two drugs work synergistically against the Tachyzoite form of T gondii.

26. Other drugs used in various combinations include:
Clindamycin:
mg/dose every 6-8 hours, maximum dose: 1.8 gm/day.
Trimethoprim + Sulphamethoxazol (Co-Trimoxazole):
160 mg/800 mg (one tablet) twice daily.
Spiramycin:
2 gr/day in two divided doses.
Azithromycin:
Loading dose 1 G (1st day), followed by 500 mg once daily for 3 weeks.

27. Oral Corticosteroids
Oral corticosteroids must be initiated at least 24 hours after starting anti parasitic drugs.

28. Therapy regimens used during Pregnancy:
Spiramycin:
2 gr/day in two divided doses.
Treatment of the Mother reduces the likelihood of Congenital transmission.

29. Standard regimen for newborns
Pyrimethamine + Sulfadiazine + Folinic acid

30. Management
Folinic acid for decreasing the likelihood of Leukopenia and Trombocytopenia.
Weekly exam of CBC and PLT.

31. Surgical Treatment Pars Plana Vitrectomy:
to remove Vitreous Opacities, or
to relieve the persistent Vitreo-Retinal traction.
Scleral Buckling:
in cases complicated with Retinal Detachment.

32. Prognosis
In cases where Optic Nerve or Macula is spared from the active disease Prognosis remains Good.

33. Poor Prognosis Profound Visual Loss: Macular Scars,
Secondary Glaucoma,
Retinal Detachment,

34. Poor Prognosis Profound Visual Loss: Macular Scars,
Secondary Glaucoma,
Retinal Detachment,
CNV.

35. TOXOCARIASIS

36. Toxocariasis is an infection caused by the accidental ingestion of:
Larvae of the Dog Round-Worm,
Toxocara Canis.

37. Children who have pica,

38. Children who are in close contact with Puppies.

39. Clinical Features
Granuloma in the Peripheral Retina and Vitreous.

40. Clinical Features Granuloma in the Peripheral Retina and Vitreous.
Posterior Pole Granuloma.

41. Clinical Features Granuloma in the Peripheral Retina and Vitreous.
Posterior Pole Granuloma.
Chronic Endophthalmitis.

42. Posterior Pole Toxocariasis
Whitish or Grayish-White in Colour

43. size of Posterior Pole Toxocariasis
Less than One Disk Diameter
Involvement of the Entire Macular Region

44. Location of Posterior Pole Toxocariasis
Juxtapapillary
Subfoveal Location

45. Diagnosis
The diagnosis of Ocular Toxocariasis is based on Clinical findings and the serological correlations.

46. Treatment
Medical treatment is directed toward the inflammatory response that produces Structural Damage and decreased vision.
This includes initial treatment with Topical or Systemic Steroids.
Antihelminthic therapy for Ocular Toxocariasis do not alter natural course of the disease.

47. Non-Infective Causes

48. Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE - AMPPE)

49. Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE - AMPPE)
Sudden,
Painless Loss of Vision,
usually Bilateral.
A flu-like prodrome consisting of Fever, Malaise and Headache precedes most cases of AMPEE.

50. Fundus Examination
Multiple Round, Circumscribed, Flat, Yellow White Sub-Retinal lesions involving the RPE.

51. Fluorescein Angiography
Early films:
Hypo-Fluorescence in Inflamed areas secondary to RPE cell Edema, Leukocyte Infiltration, and Capillary Nonperfusion.

52. Fluorescein Angiography
Late films:
Hyperfluorescence due to leakage from the Choriocapillaris through damaged RPE cells.

53. As these lesions resolve over several weeks, vision improves in most cases to slightly less than initial acuity.

55. Management Neurologic and Systemic Evaluation.
Macular involvement in AMPPE needs treatment with Systemic Steroids.
Prompt use of Systemic Steroids rapidly resolves inflammation, and may result in a better visual prognosis.

56. Multiple Evanescnt White Dot Syndrome (MEWDS)

57. Multiple Evanescnt White Dot Syndrome (MEWDS)
Multiple, Small, Discrete , White dots, Located in Deep Retina or RPE.

58. Multiple Evanescnt White Dot Syndrome (MEWDS)
Distributed mainly in Perifoveal and
Peripapillary regions.

59. Multiple Evanescnt White Dot Syndrome (MEWDS)
Hyperemia or Edema of Optic Disc common.
Disc Capillary Leakage with Staining

60. Fluorescein Angiography
Early: Hyperfluorescence.
Late:
Staining of lesions at RPE level.

61. Prognosis Excellent: Most back to 20/20. Recover time: 1-16 weeks.
Recurrences: Rare.

62. Serpiginous Choroiditis

63. Serpiginous Choroiditis
Bilateral Inflammatory Disorder.
Grayish-White lesions at RPE or Choroidal level.

64. Serpiginous Choroiditis
Usually occurs in the Peripapillary region and progresses in a Helicoid or Serpiginous manner toward the Macula.
Acute lesions occur at the edge of the Chronic lesion.
Recurrences are common.

65. Serpiginous Choroiditis
Chronic lesions show Pigmentary changes.

66. Birdshot Retinochoroidopathy (BSRC)

67. Birdshot Retinochoroidopathy (BSRC)
Gradual Painless Visual Loss,
Floaters,
Photophobia,
Nyctalopia, and
Disturbances in Color Vision.
The diagnosis of BSRC is Clinical.

68. Multiple Depigmented Spots,
White or Cream-colored,
Oval or Round,
At the level of the RPE and Choriocapillaries.

69. Usually distributed around the Optic Nerve head and Radiate toward:
the Periphery specially Inferior and Nasal.

70. May become Confluent resulting in larger Geographic areas of Hypopigmentation.

71. Fluorescein Angiographic
Hypofluorescent on Early.
Hyperfluorescent on Late frames.

72. CME

74. Epiretinal Membranes

76. Thank You