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   Table of Contents      
ARTICLES
Year : 1984  |  Volume : 32  |  Issue : 6  |  Page : 539-543

Cystoid macular oedema


Sankara Nethralaya Medical Research Foundation, 18 College Road, Madras, India

Correspondence Address:
Mathivanan Natarajan
Sankara Nethralaya Medical Research Foundation, 18 College Road, Madras-6
India
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Source of Support: None, Conflict of Interest: None


PMID: 6599901

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How to cite this article:
Natarajan M, Abraham C, Badrinath S S. Cystoid macular oedema. Indian J Ophthalmol 1984;32:539-43

How to cite this URL:
Natarajan M, Abraham C, Badrinath S S. Cystoid macular oedema. Indian J Ophthalmol [serial online] 1984 [cited 2019 May 20];32:539-43. Available from: http://www.ijo.in/text.asp?1984/32/6/539/30864

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Table 5

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Table 1

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Table 1

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Cystoid macular oedema is a term applied to the accumulation of fluid in the cystoid spaces in the external plexiform layer of the retina. On fluorescein angiography fluorescein leaks into these spaces giving a charac­teristic stellate or honey-combed appearance. It is well known that cystoid macular oedema can be caused by several ocular disorders and there are several publications dealing with either one or more aspects of the condition and its management. This study will deal in detail the fluorescein angiography findings particularly in the mid arterio-venous phase, the visual impairment in this condition and the results of argon laser photocoagulation in eyes with cystoid macular oedema associa­ted with vascular retinopathies. The varied associated ocular conditions that have been responsible for cystoid macular oedema will also be described.


  Material and methods Top


The records of 140 patients (168 eyes) with a diagnosis of cystoid macular oedema were evaluated. In 58 eyes (52 patients) the diagnosis was doubtful or inadequately documented. These eyes were eliminated leaving 109 eyes of 88 patients for study. 62 were males and 26 females, their age rang­ing from less than 20 years to more than 50. Fluorescein angiographic documentation was obtained in 76 eyes and fluorescein opthal­moscopy was performed in 14. The diagno­sis was based on ophthalmoscopy in the remaining. Argon laser photocoagulation was performed in 40 eyes. In 20 eyes with either discrete micro-vascular abnormalities or circinates in the perifoveal region, treat­ment was directed towards these lesions. The centres of the circinates were coagulated. Lesions within 300 microns of the perifoveal net were not treated. Most of these eyes had diabetic retinopathy. The C-pattern of treatment was employed in 3 eyes and treatment was placed in hypoxic areas in the perifoveal region in 2. A 100 or 200 micron spot size, an exposure time of 0.05 or 0.1 sec. and the power adjusted to produce adequate coagulation was used. In the remaining eyes photocoagulation was in the form of a panretinal photocoagulation using the 500 micron spot size and an exposure time of 0.1 sec. and suitable power to produce modera­tely intense coagulation. These were mostly eyes with proliferative or pre-proliferatives diabetic retinopathy, Eales' disease or a central retinal vein occlusion. Eyes with branch retinal vein occlusion received a seg­mental panretinal photocoagulation. 20 patients who had associated ocular inflammation received oral cortico-steroids either as a single dose (6) or in divided doses (14) for a period of one week to over 6 months.

Follow-up fluorescein angiography was done in 27 eyes. All patients have been followed up for a period of I month to over a year. [Table - 1]

Fluorescein angiographic features

In the early arterio-venous phase 18 eyes showed no abnormality in the region of the macula. In 42 eyes the perifoveal capillary network was abnormally dilated. Micro­aneurysms or intraretinal microvascular abnormalities were demonstrable in 44 eyes. The perifoveal capillary net was found to be disrupted in 8 eyes and 5 eyes showed foveal hypoxia of varying extent.

In the mid arterio-venous phase dilatation of the perifoveal net in another 6 eyes and intraretinal microvascular abnormalities in another 6 became apparent. Leakage of fluorescein from these abnormal perifoveal capillaries had commenced in 66 eyes. In the remaining leakage was evident only in the later phases.

In the delayed phase (10 minutes after I.V. fluorescein) the macula stained intensely in 19 eyes, moderately in 44 and minimally in 13. In all instances the typical pattern of cystoid macular oedema was observed. The delayed staining involved all the 4 quadrants around the fovea in 72 eyes. It was partial in 4 eyes-involving 2 quadrants in 3, and 3 quadrants in l. [Table - 5] shows the relation­ship of visual acuity to the degree of macular straining.

Results of Photocoagulation

Of the 40 eyes which were subject to photocoagulation the distant visual acuity in 10 improved, and in 13 deteriorated. The deterioration was not due to photocoagula­tion in any eye. 17 eyes maintained their visual acuity. Near vision improved in 9, deteriorated in 10 and was maintained in 21. Of the 23 eyes in which funds fluorescein angiogram was repeated after photocoagula­tion 10 eyes showed a decrease in size of the perifoveal capillary net, which was evident in the early or mid arterio-venous phase. There was improvement in capillary perfusion in 1 eye which previously showed hypoxia. 9 eyes showed no change when compared to the pre-photocoagulation angiogram. The quantum of dye leakage in the mid arterio­venous phase was diminished in 13 eyes. In the delayed phase, 4 eyes showed complete regression of cystoid macular oedema while 14 showed the staining of the macula to be less intense. There was no appreciable change in 5 eyes.


  Discussion Top


The visual impairment in cystoid macula oedema can be varied. However, 16 eyes with a visual acuity range of 6/5-6/9 for dis­tance and 36 eyes with N/5-N/8 for near tell us that a person can have good visual acuity despite cystoid macular oedema. The quantum of fluorescein leakage as indicated by the degree of staining of the macula in the delayed phase seem to have no significant bearing on the patients' visual acuity.

We see in this series that a consistent finding in the arterio-venous phase of the fluorescein angiogram is dilatation of the perifoveal capillary net. This finding was observed irrespective of the cause for cystoid macular oedema. We believe that whether the cause is inflammatory, traction by vitreous or an associated disease in the macula or fundus periphery involving either the retina or choroid, the perifoveal capilla­ries become susceptible to dilatation and became incompetent. This may indicate a peculiar vulnerability of the perifoveal net. In cases where there is vitreous make them functionally incompetent. In cases of inflam­mation particularly in sites remote from the macula as in pars planitis or anterior uveitis it is possible that toxic factors operate and the perifoveal capillary net undergoes changes merely because it is more vulnerable. It would be worthwhile studying the peripheral capillary network in these instances. In con­dition like choroidal folds or choroidal haemangiomas it is likely that these conditions act as a stimulus to capillary dilatation and incompetence. When discrete microvascular abnormalities are present in the region of the macula, they alone can give rise to cystoid macular oedema. The absence of any abnor­mality in the early A.V. phase of 18 eyes indicate that functional derangement of the perifoveal capillary net can occur in the absence of any demonstrable structural change. It is also interesting to note the occurrence of cystoid macular oedema in eyes where foveal non-perfusion was evident. The decrease in size of the perifoveal capillary net in 11 eyes following photocoagulation the improvement in perfusion in 1, decreased leakage of dye in 14 with less intense staining and complete regression of cystoid macular oedema in 5 tell us that the process may be reversible. Our technique of photocoagula­tion was directed to the associated cause of cystoid macular oedema and only in 3 eyes we employed a C-pattern.

The visual results show that though there is scope for regression of the condition followed by improvement in vision, a vast majority of patients either showed no improvement or worsened. Eyes where vision improved were mainly those in which a specific treatable disorder (like the vascular retinopathies) was associated with cystoid macular oedema.


  Summary Top


The visual impairment, detailed fluorescein angiographic features before and after laser photocoagulation, the results of photocoagu­lation and the condition responsible for cystoid macular oedema in 109 eyes of 88 patients is discussed. The consistent findings seen in the A.V. phase of the angiogram irrespective of the activity of cystoid macular oedema is dealt with in detail[10].

 
  References Top

1.
Bon S Fine and Alexander J Brucker, 1981, Cystoid Macular Oedema; Amer J. Ophthalmol; 92: 466.  Back to cited text no. 1
    
2.
Gass J.D.M. and Norton E.W.D., 1966, Arch. Ophthalmol 76, 646.  Back to cited text no. 2
    
3.
Gass JDM, 1970, Sterioscopic atlas of Macular disease-A Funduscopic and angiographic presenta­tion; 150-151.  Back to cited text no. 3
    
4.
Gass JDM 1977, Sterioscopic atlas of macular disease-diagnosis and treatment-Second edition; 250-259.  Back to cited text no. 4
    
5.
Lawrence A Tannuzzi and Richard M Klein 1974, Amer J. Ophthalmol. 84:517.  Back to cited text no. 5
    
6.
Lobes LA Junior and MG Grand; 1980, Archives of Ophthalmology; 98: 1230.  Back to cited text no. 6
    
7.
Richard M Klein and Lawrance Yannuzzi 1976, Cystoid Macular Edema in the 1st week after cataract extraction; AJO; 81; 614.  Back to cited text no. 7
    
8.
Schatz H, 1976, Archives of Ophthalmology; 94; 761.  Back to cited text no. 8
    
9.
Schatz H., 1978, Interpretation of Funds Fluorescein Angiography; The CV Mosby Co..  Back to cited text no. 9
    
10.
Zweng HC; 1977, Argon Laser Photocoagula­tion. The CV Mosby Co.  Back to cited text no. 10
    



 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6]



 

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