Cystoid macular oedema

Cystoid macular oedema

1. CYSTOID MACULAR OEDEMA PRESENTER : Dr. Rujuta MODERATOR : Dr. Archis Shedbale

2. DEFINITION A pathological response of the retina consisting of fluid accumulation in the outer plexiform layer of central macula that results in the formation of visible cystic spaces.

3. HISTORICAL REVIEW Post cataract Cystoid Macular Oedema was initially reported in 1953 by Irvine. Gass described macular oedema in 1966

4. INCIDENCE 60% of uncomplicated cases of intracapsular cataract extraction 20% of uncomplicated cases of extracapsular cataract extraction 10-20% of uncomplicated phacoemulsification cases

5. PATHOGENESIS Vitreomacular traction Inflammation

6. PATHOGENESIS continued… VITREOMACULAR TRACTION: Incomplete posterior vitreous detachment Anterior to posterior traction on macula Development of Cystoid Macular Oedema

7. PATHOGENESIS continued… INFLAMMATION: Ischaemia and inflammation Intravitreal cytokine release Increased permeability of retinal vascular endothelium Development of Cystoid Macular Oedema

8. PATHOLOGY Electron microscopy shows intracellular accumulation of fluid producing cystoid areas and swelling of Muller’s cells : reversible stage Excess fluid may break through cell membrane and accumulate extracellularly : irreversible stage

9. RISK FACTORS POSTOPERATIVE: Most commonly after cataract surgery Highest risk after inadvertent rupture of posterior capsule and/or persistent traction to anterior segment structures Also seen after penetrating keratoplasty , scleral buckling, laser iridotomy , cryotherapy for retinal break, panretinal photocoagulation

10. RISK FACTORS continued… DIABETIC RETINOPATHY: Due to vascular compromise CME occurs along with diffuse macular oedema Associated microaneurysms and hard exudates are often evident

11. RISK FACTORS continued… RETINAL VEIN OCCLUSIONS: Both branch and central vein occlusion can result in severe macular oedema Due to increased intravascular hydrostatic pressure leading to hypoxic capillary endothelial damage and fluid extravasation Release of intravitreal cytokines VEGF, Interleukin 6, Pigment epithelium-derived factor

12. RISK FACTORS continued… CHOROIDAL NEOVASCULAR MEMBRANE: Exudation of fluid from the capillaries of CNVM

13. RISK FACTORS continued… COAT’S DISEASE: Unilateral condition occurring more commonly in males Presence of retinal telangiectasias Anomalous retinal vasculature produces leakage with resultant cystoid and diffuse macular oedema

14. RISK FACTORS continued… RADIATION INDUCED CME: Patients receiving radiation treatment involving the head and neck may develop radiation retinopathy 6months to 3 years later Depends on total dose and daily fraction Most commonly after doses of 30-35Gy Usually bilateral

15. RISK FACTORS continued… RETINAL ARTERY MACROANEURYSMS: Acquired disorder Often multiple May thrombose and close spontaneously Laser treatment may be given

16. RISK FACTORS continued… TUMOURS: Choroidal tumours such as naevi , malignant melanoma, cavernous haemangiomas Cystoid changes occur as a lack of oxygenation of retinal tissue

17. RISK FACTORS continued… INFLAMMATIONS: Idiopathic uveitis Birdshot chorioretinopathy Sarcoidosis Toxoplasmosis Posterior scleritis Harada’s syndrome Behçet’s syndrome

18. RISK FACTORS continued… MEDICATIONS: Topical epinephrine (reduced blood flow in the retina and choroid) Nicotinic acid Latanoprost (PGs like action)

19. OCULAR MANIFESTATIONS SYMPTOMS: Decreased central visual acuity Metamorphopsia Micropsia Scotomata Ocular irritation Photophobia Conjunctival Injection

20. OCULAR MANIFESTATIONS 90D EXAMINATION: Blurring of normal RPE and choroidal background Pockets of fluid in the outer plexiform layer Largest pockets centrally, progressively smaller cysts peripherally Yellow spot (diffusion of luteal pigment) evident in the central macula Small intraretinal and intracystic haemorrhages , microaneurysms , telangiectasias may be seen

21. OCULAR MANIFESTATIONS OTHER FINDINGS: Post cataract surgery aqueous and/or vitreous cells and flare Ruptured anterior hyaloid face Vitreous traction to anterior segment structures

22. OCULAR MANIFESTATIONS Rupture of inner retinal cyst can occur to give rise to a lamellar macular hole Prolonged CME may induce atrophy of macular photoreceptors

23. FUNDUS FLUORESCEIN ANGIOGRAPHY Typical petalloid pattern in the central macula secondary to dye leakage from perifoveal capillaries The dye accumulates in the cystic spaces in the outer plexiform layer Leakage from the disc and retinal vessels in the late stage

24. Early phase fluorescein angiography of a patient with non-proliferative diabetic retinopathy. Microaneurysms are seen most prominently temporal to the fovea in addition to fluorescein leakage in the foveal avascular zone. Late-phase FA of the same patient showing diffuse leakage temporal to and within the foveal avascular zone corresponding to diabetic macular edema.

25. OPTICAL COHERENCE TOMOGRAPHY Directs a beam of near infrared light (830-nm) perpendicular to the surface of the retina and analyzes the properties of the reflections. These images can display and even measure the thickened, cystic retina found in edematous areas. It is also useful in visualizing the properties of the vitreoretinal interface and effectively demonstrates role of vitreous traction in the formation of CME

26. A. Color fundus photograph of the left eye of a patient with non-proliferative diabetic retinopathy and lipid exudation in and around the fovea. B. Late-phase FA reveals macular edema in the central macula. C. Optical coherence tomography demonstrates the abnormal vitreoretinal interface as well as macular edema.

27. OPTICAL COHERENCE TOMOGRAPHY Shows central cysts, loss of foveal depression and macular thickening Test of choice for diagnosis and follow up of patients with CME

28. RETINAL THICKNESS ANALYZER The retinal thickness analyzer is a non-contact imaging technique that allows for quantification of retinal thickness.

29. MANAGEMENT MEDICAL TREATMENT: NSAIDs: Topical non-steroidal anti-inflammatory medications are the most common treatment for ME following cataract surgery. These agents decrease intraocular prostaglandin levels, which have been implicated in the pathogenesis of ME.

30. MANAGEMENT continued… Diclofenac 0.1% and ketorolac 0.5% ophthalmic solutions are the only topically applied NSAIDs specifically approved by the Food and Drug Administration for this indication.

31. MANAGEMENT continued… MEDICAL TREATMENT: CORTICOSTEROIDS : Locally, decrease intracellular and intercellular oedema , suppress macrophage activity, and decrease lymphokine production Systemically, sequester T cells out of circulation (inhibiting cytotoxic and recruitment functions) and decrease phagocytic activity of polymorphonuclear leukocytes

32. MANAGEMENT continued… Mode of delivery of corticosteroids: Topical eye drops Posterior sub tenon’s injections Intravitreal Systemic- oral and intravenous routes

33. MANAGEMENT continued… Relative potency of topical corticosteroids in decreasing order: 1. Dexamethasone 0.1% 2. Prednisolone 1% 3. Fluorometholone 0.1% 4. Rimexolone 1% 5. Loteprednol 0.5% 6. Medrysone 1%

34. MANAGEMENT continued… POSTERIOR SUB TENON’S INJECTIONS: Sub- Tenon's injections offer an alternative to deliver relatively high doses of corticosteroids to the eye with lower risks of systemic complications. Risks of this procedure include persistently elevated intraocular pressure, and intraocular penetration.

35. MANAGEMENT continued… INTRAVITREAL TRIAMCINOLONE ACETONIDE: The use of intravitreal injection of triamcinolone acetonide ( Tricort ) has increased due to its potent ability to ameliorate refractory ME secondary to diabetes mellitus, retinal venous occlusions, inflammation, and other idiopathic causes. The effect is temporary and typically lasts for three to six months, the ME usually responds to re-injection.

36. Optical coherence tomography image of an eye with diabetic macular edema with corresponding retinal thickness map generated by the OCT. OCT of the same patient one month following intravitreal triamcinolone acetonide injection withcorresponding retinal thickness map.

37. MANAGEMENT continued… MEDICAL TREATMENT: ACETAZOLAMIDE: Facilitates the transport of water across the RPE from subretinal space to choroid

38. MANAGEMENT continued… LASER TREATMENT: Focal/grid laser photocoagulation is used in the treatment of diabetic ME. It promotes the formation of tight junctions between RPE cells as well as reduces oxygen demand from photoreceptors and increase oxygen perfusion from the choroid.

39. MANAGEMENT continued… ANTI VEGF AGENTS: VEGF increases vascular permeability by relaxing endothelial cell junctions, which increases permeability and leakage. Inhibition of VEGF blocks this effect to some extent anti-VEGF molecules pegaptanib , ranibizumab , and bevacizumab are in use.

40. MANAGEMENT continued… SURGICAL TREATMENT: YAG laser to release adhesions between vitreous and undersurface of cataract wound, iris or the intraocular lens implant Vitrectomy IOL explantation