cystoid macular oedema

CYSTOID MACULAR OEDEMAPRESENTER : Dr. Rujuta MODERATOR : Dr. Archis

Shedbale

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.

HISTORICAL REVIEW

Post cataract Cystoid Macular Oedema was initially reported in 1953 by Irvine.

Gass described macular oedema in 1966

INCIDENCE

60% of uncomplicated cases of intracapsular cataract extraction

20% of uncomplicated cases of extracapsular cataract extraction

10-20% of uncomplicated phacoemulsification cases

PATHOGENESIS

Vitreomacular tractionInflammation

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VITREOMACULAR TRACTION:Incomplete posterior vitreous detachment

Anterior to posterior traction on macula

Development of Cystoid Macular Oedema

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INFLAMMATION:Ischaemia and inflammation

Intravitreal cytokine release

Increased permeability of retinal vascular endothelium

Development of Cystoid Macular Oedema

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

CYSTOID MACULAR OEDEMA

Pseudophakic Non-Pseudophakic

Diabetic Retinopathy

Retinal Vein Occlusions

Choroidal Neovascular Membrane

RISK FACTORS

POSTOPERATIVE:Most commonly after cataract surgeryHighest 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

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DIABETIC RETINOPATHY:Due to vascular compromiseCME occurs along with diffuse macular

oedemaAssociated microaneurysms and hard

exudates are often evident

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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

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CHOROIDAL NEOVASCULAR MEMBRANE:

Exudation of fluid from the capillaries of CNVM

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COAT’S DISEASE:Unilateral condition occurring more

commonly in malesPresence of retinal telangiectasiasAnomalous retinal vasculature produces

leakage with resultant cystoid and diffuse macular oedema

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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 fractionMost commonly after doses of 30-35GyUsually bilateral

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RETINAL ARTERY MACROANEURYSMS:Acquired disorderOften multipleMay thrombose and close spontaneouslyLaser treatment may be given

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TUMOURS:Choroidal tumours such as naevi, malignant

melanoma, cavernous haemangiomasCystoid changes occur as a lack of

oxygenation of retinal tissue

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INFLAMMATIONS:Idiopathic uveitisBirdshot chorioretinopathySarcoidosisToxoplasmosisPosterior scleritisHarada’s syndromeBehçet’s syndrome

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MEDICATIONS:Topical epinephrine (reduced blood flow in

the retina and choroid)Nicotinic acidLatanoprost (PGs like action)

OCULAR MANIFESTATIONS

SYMPTOMS:Decreased central visual acuityMetamorphopsiaMicropsiaScotomata Ocular irritationPhotophobia Conjunctival Injection

OCULAR MANIFESTATIONS

90D EXAMINATION:Blurring of normal RPE and choroidal

backgroundPockets of fluid in the outer plexiform layerLargest pockets centrally, progressively

smaller cysts peripherallyYellow spot (diffusion of luteal pigment)

evident in the central maculaSmall intraretinal and intracystic

haemorrhages, microaneurysms, telangiectasias may be seen

OCULAR MANIFESTATIONS

OTHER FINDINGS:Post cataract surgery aqueous and/or

vitreous cells and flareRuptured anterior hyaloid faceVitreous traction to anterior segment

structures

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

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

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.

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

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.

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

RETINAL THICKNESS ANALYZER

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

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.

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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.

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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

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Mode of delivery of corticosteroids:Topical eye dropsPosterior sub tenon’s injectionsIntravitrealSystemic- oral and intravenous routes

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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%

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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.

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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.

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.

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MEDICAL TREATMENT:ACETAZOLAMIDE:Facilitates the transport of water across the

RPE from subretinal space to choroid

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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.

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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.

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SURGICAL TREATMENT:YAG laser to release adhesions between

vitreous and undersurface of cataract wound, iris or the intraocular lens implant

VitrectomyIOL explantation