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? A diffuse pattern of macular thickening and fluid accumulation, with or without associated haemorrhages and exudates (see also Diabetes - macular oedema)
? A cystic accumulation of fluid within the retina, centred around the macula, known as cystoid macular oedema (CMO). CMO occurs in a variety of ocular conditions that increase vascular permeability, thought to arise in some cases due to prostaglandin-mediated inflammation. CMO is more common after surgical complications, for example, posterior capsule rupture with damage to the vitreous
? Retinal traction in the macular area (see also Vitreomacular traction syndrome).
CLASSIFICATION
?Vascular disease - Diabetic retinopathy, Retinal vein occlusions, Hypertensive retinopathy, Radiation retinopathy, Choroidal neo-vascularisation
?Ocular inflammatory disease - Uveitis, Retinal vasculitis,
?Postoperative - Aphakic/pseudophakic CMO, laser treatment
?Retinal degenerations and Inherited dystrophies - Age-related macular degeneration, Retinitis pigmentosa
?Drug-induced - prostaglandin analogues, dipivefrin and adrenaline
?Vitreous traction - Epiretinal membrane, Vitreomacular traction syndrome
?Intraocular tumours.
SYMPTOMS
Decreased central vision may be a history of recent ocular surgery.
SIGNS
Visual acuity is usually reduced and the foveal light reflex often appears irregular. Slit-lamp biomicroscopy reveals loss of the foveal depression, retinal thickening, and there may be multiple small cysts in the foveal region. Optic nerve head swelling or intra-retinal haemorrhage may be present. In severe, chronic cases of CMO, cysts occasionally coalesce, resulting in the formation of a lamellar macular hole and permanent damage to central vision. The examination should also include a search for evidence of associated conditions, for example, uveitis, choroidal melanoma or surgical complications.
PREVALENCE
Common.
SIGNIFICANCE
Prolonged oedema increases the risk of permanent retinal damage and visual loss.
DIFFERENTIAL DIAGNOSIS
Macular hole, Central serous chorioretinopathy, Choroidal neovascularisation.
SEE ALSO
Conditions listed under classification, above.
MANAGEMENT
Additional investigations
Fluorescein angiography of CMO characteristically shows dye leakage around the fovea, in a petaloid (flower petal) configuration due to the radial arrangement of nerve fibres around the fovea. Other pathological changes such as choroidal neovascularisation (CNV) may be evident. Optical coherence tomography (OCT) enables non-invasive confirmation of macular oedema and may show vitreous traction or CNV.
Advice
The underlying cause, if present, is treated appropriately. For example, medications such as topical prostaglandin analogues may require cessation. In many cases (for example, pseudophakic CMO), a high rate of recovery is expected, and no specific treatment is required. The incidence of symptomatic CMO after cataract surgery has fallen since the introduction of phacoemulsification and extracapsular procedures.
Topical medications
In general, therapeutic intervention in postoperative CMO is appropriate in prolonged disease (over six months), and in high-risk patients with pre-existing inflammatory eye disease or prior history. Topical non-steroidal anti-inflammatory agents (NSAIDs) - for example, diclofenac 0.1 per cent, or ketorolac 0.5per cent qid or corticosteroids such as prednisolone 1 per cent qid are common first-line agents. Their effect may be attributable to a blockade of prostaglandin synthesis.
Laser treatment, incisional surgery
Depending on the cause, duration and severity of macular oedema, indicated treatments may include oral medications (NSAIDs, corticosteroids or acetazolamide), intravitreal steroids (such as triamcinolone), laser treatment and vitrectomy.
See the management sections in the respective conditions.