CYSTOID MACULAR EDEMA (CME)

It refers to collection of fluid in the outer plexiform
(Henle’s layer) and inner nuclear layer of the retina,
centred around the foveola.
Etiology
It is associated with a number of disorders. A few
common causes are as follows:
1. As postoperative complication following cataract
extraction and penetrating keratoplasty.
2. Retinal vascular disorders e.g., diabetic
retinopathy and central retinal vein occlusion.
3. Intraocular inflammations e.g., pars planitis,
posterior uveitis, Behcet disease.
4. As a side-effect of drugs e.g., following use of
adrenaline eyedrops, especially for aphakic
glaucoma.
5. Retinal dystrophies e.g., retinitis pigmentosa.
Pathogenesis
CME develops due to leakage of fluid following
breakdown of inner blood-retinal barrier (i.e., leakage
from the retinal capillaries).
Clinical features
1. Visual loss. Initially there is minimal to moderate
loss of vision, unassociated with other symptoms.
If oedema persists, there may occur permanent
decrease in vision.
2. Ophthalmoscopy in clinically established cases
reveals a typical ‘Honey-comb appearance’ of
macula (due to multiple cystoid oval spaces) (Fig.
11.24). CME is best examined with a fundus
contact lens on slit-lamp or +90D lens.
3. Fundus fluorescein angiography demonstrates
leakage and accumulation of dye in the macular
region which in a well-established case presents
a ‘flower petal appearance’ (Fig. 11.25).
Complications
Long-standing CME may end in lamellar macular hole.
Treatment
1. Treatment of the causative factor, e.g.,
photocoagulation for diabetic CSME; cessation of
causative topical 2% adrenaline eye drops, so on.
2. Topical antiprostaglandin drops like
indomethacin or flurbiprofen, used pre and postoperatively,
prevent the occurrence of CME
associated with intraocular surgery.
3. Topical and systemic steroids may be of some
use in established cases.
4. Systemic carbonic anhydrase inhibitors (CAIs)
e.g., oral acetazolamide may be beneficial is some
cases of CME