|Year : 1983 | Volume
| Issue : 3 | Page : 140-142
Cystoid macular oedema
Deptt. of Ophthal., Medical College, Amritsar, India
Deptt. of Ophthal., Medical College, Amritsar
|How to cite this article:|
Singh D. Cystoid macular oedema. Indian J Ophthalmol 1983;31:140-2
Cystoid macular oedema is an accumulation of fluid within Henle's fibre layer of the fovea, causing a thickening of the retina in a characteristic cystic pattern. It occurs most commonly following cataract extraction, but it may be seen in any condition that causes an abnormal increase in perifoveal capillary permeability.  The patient with cystoid maculopathy presents with a decreased visual acuity, a positive central scotoma and metamorphopsia.
The present study
It concerns the cases of cystoid macular oedema (CME) encountered in a series of 650 cases of intraocular lens implants, 100 cases of routine intracapsular cataract extraction (ICCE) and 100 cases of extracapsular cataract extraction (ECCE) done by microsurgical technique. The observation period for I.O.L. cases varied from 4 months to 60 months, while the non-implant cases have been followed for about 1 year.
[Table - 1] shows the breakup of I.O.L. cases under study.
All intracapsular cataract extractions with or without intraocular lens were done by Amritsar method.  All extracapsular cataract extractions were done by microsurgery  as follows: An irrigating cystotome was introduced through a 3 mm limbus incision and the anterior capsule was incised. The nucleus of the lens was separated from the cortex by the same cystotome. The incision was then extended with a scissors. The nucleus was delivered after which the cortical matter was removed by irrigation with or without aspiration.
Diagnosis of CME:
The diagnosis of CME is based on many clinical observations. The retina shows loss of foveal depression with ophthalmoscope and outline of multiple cystic spaces retroilluminated with slit lamp. Often a yellow exudate lies deep within or beneath the retina in the foveal area. Splinter haemorrhages may be seen.
The vitreous may be found adherent to the cataract wound and inflammatory cells may be ,found in it.
There may be other findings like anterior chamber flare, disc oedema and perilimbal injection.
Fluorescein angioscopy will show typical leak pattern.
[Table - 2] shows the details of I.O.L. patients who developed cystoid macular oedema.
[Table - 3] shows the details of non-implant CME cases.
There were no cases of CME in the ECCE group during the period of observation.
| Disccussion|| |
Following cataract extraction, there is usually a delay of weeks and months before the onset of CME. If all the patients are routinely studied with fluorescein angiography after surgery, some 40 to 50% may be seen to have CME, but it is only 2-3% of the cases that the condition is severe enough to present as a clinical problem. 
It is well recognized that the incidence of CME is higher after ICCE than after ECCE. 
Worst  (1917) described a cisternal system in the vitreous, which he thought was essential for the physiological function of macula by allowing fluid transport through the vitreous. He has described channels which connect the spaces before the macula and the optic disc to the anterior surface of the vitreous. The zonule and the posterior capsule of the lens act as a barrier between the anterior and the posterior segments of the eye. After ICCE the way is open for the noxious agents to travel directly to the macular area and produce reactive changes like CME.
Our I.O.L. cases showing CME belonged mostly to the group ICCE receiving Shah iris clip lenses (11.9%). In most cases the visual loss was great and recovery did not occur. Such occurences have not been observed with other lenses. It is quite likely that potentially toxic materials have been used in the making of Shah iris clip lenses. Only that can explain the postoperative complications that occured with these lenses.  The incidence of CME with Shah iris clip lenses after ECCE was not high (1.8%). That highlights the role of posterior capsule in the protection of macula.
Cystoid macular oedema can be extremely frustrating to the surgeon. However a great majority of the patients would show a spontaneous recovery over a period of 6 months. If there are signs of inflammation, it should receive appropriate attention. Topical steroids are not enough. Periocular injection of depot form of steroid should be given. Oral prostaglandin inhibitors like indomethacin have been used but have not proved useful in established cases of CME. Vitrectomy may be indicated in patients who have vitreous adherent to the wound and who show improvement with steroids.
The overall incidence of CME in our cases with I.O.L. is very low, a fact which is hard to believe. How to explain it? Is it a racial characteristic that more pigmented people are less prone to CME after I.O.L.? Perhaps there is a need for a more sophisticated study in this direction.
| References|| |
|1.||Fraunfelder, r.T., and Roy, F.H., Current Ocular Therapy, 1930, W.B. Saunders Company, Philadelphia, U.S.A., p. 517. |
|2.||Singh, D., Nirankari, M.S., and Singh M., Proceedings All India Ophthal. Soc., 1977, p. 23. |
|3.||Olmos, E., Roy, F.H., and Singh, D., Intraocular Lenses. Praeger Publishers, New York, p. 35, 1981. |
|4.||Moss, L., Am. Intraocular Implant Soc. J., 5, 326, 1978. |
|5.||Worst, J.G.F., Trans. Ophth., Soc. U.K., 97, 550, 1977. |
|6.||Singh, D., Singh, M., and Singh, A., Proceedings of All India Ophthalmological Conference, p. 42, 1977. |
[Table - 1], [Table - 2], [Table - 3]