|Year : 1983 | Volume
| Issue : 7 | Page : 878-881
Fellow eye in senile disciform degeneration of the macula
Rajvardhan Azad, HK Tewari, PK Khosla
Dr. Rajendra Prasad Centre for Ophthalmic Sciences AIIMS, New Delhi, India
Dr. R.P. Centre for Ophthalmic Sciences AIIMS, New Delhi-29
|How to cite this article:|
Azad R, Tewari H K, Khosla P K. Fellow eye in senile disciform degeneration of the macula. Indian J Ophthalmol 1983;31:878-81
|How to cite this URL:|
Azad R, Tewari H K, Khosla P K. Fellow eye in senile disciform degeneration of the macula. Indian J Ophthalmol [serial online] 1983 [cited 2013 May 22];31:878-81. Available from: http://www.ijo.in/text.asp?1983/31/7/878/29691
Senile disciform Degeneration of macula is one of the various ill-defined entities which destroy central vision and their diagnosis is merely a satisfaction of old age. Usually nothing much can be done for the patient in the last stage of the disease but examination of the normal (fellow) eye may reveal a wide spectrum of changes which might be preceding the development of a full-fledged picture of disciform degeneration and may be amenable to treatment.
We present our experience of detailed clinical examination and fluorescein angiography of fellow eyes of 50 cases with a view to understanding various precursor lession and to suggest the possible stages where therapeutic intervention can be done.
| Material and method|| |
Fifty patients diagnosed clinically and supported by fluorescein angiography as Senile Disciform Degeneration of macula from Retina, Service of Dr. Rajendra Prasad Centre for Ophthalmic Sciences were included in the study. Fellow eyes were subjected to thorough clinical examination colour fundus photography and fluorescein angiography. The patients were divided in three groups on the basis of fluorescein angiographic examination, i.e. UN=unilateral disciform with normal fellow eye, UD=unilateral discifonn with probable precursor lesions in fellow eye and BL=bilateral disciform degeneration.
| Observations|| |
[Table - 1] shows age and sex distribution indicating an average age of over 55 years and male predominance. [Table - 2] shows distribution of refractive error- Hypermetropia being the commonest. Absence of Aphakia in this series was significant. No systemic disease association was seen in majority of cases [Table - 3]. [Table - 4] shows clinical and fluorescein angiographic findings in the fellow eyes.
| Discussion|| |
Senile disciform macular degeneration also being called senile exudative macular degeneration occurs in 25-40% of cases over the age of 60 years and forms the most important chorioretinal cause of impaired central vision in this age group.
This series had an average of 55.5 years (range 40 to 74 years) which is comparable to findings of Chandra et al who reported average age of 60 years (range 40 to 87 years). Male predominance (Male 80%, Female 20%) in our series is contrary to findings of Chandra et al who found equal affection of both sexes. Males being bread earners in our society may be coming more for examination due to their concern about vision. Lesions appear at a later age group in males although the difference is not significant. Examination of fellow eye indicated that 16% had no lesion, 56% had some lesion while 30% had fullfledged picture. An increase in age bracket from UN group normal fellow eye (49.4 years) to UD group-probable precursor lesions in fellow eye (56.43 years) to BL group-bilateral involvement (60.8 years) revealed that the disease is a progressive one. We have also observed in follow up of UD group cases that precursor lesions develop into full fledged picture in an average of 3 years.
Hypermetropic eyes may be more prone to senile macular disciform degeneration as majority of patients (55%) had hypermetropia. A significant finding is absence of aphakes and this inverse relationship may possibly be due to the different pathogenetic factors for senile macular degeneration and cataract. It is interesting that nuclear cataract was also not seen and fluorescein angiography was possible in all cases.
Prevalence of diabetes was high (21.74%) in our cases which is much more than the prevalence of diabetes in that age group in our population. So it is surmised that diabetes may be playing some part in its aetiopathology may be by inducing more arteriosclerotic changes. Some cases were diagnosed outside as diabetic maqulopathy but these turned out to be classical disciform degeneration in one eye with colloid degeneration in the other eye on fluorescein angiography. It is thus seen that association of diabetes in such cases must be looked for.
Hypertension in the form of arterial diseases has been found to be a common association but is not corroborated by our findings. Proneness to develop disciform lesion may be more with diabetes as 21.74% had this association and many of them showed background diabetic retinopathy.
Fluorescein angiography revealed lesions in fellow eyes which could be interpreted as various stages. The lesions seen were drusens scattered or confluent, pigment epithelial detachment subretinal neovascularisation, haemorrhage and exudation and mound formation. The staging was done keeping in view the progressive development of lesions associated with functional changes in vision.
Scattered drusens were considered as early precursor lesions. These consisted of drusens ofvarying sizes and shapes often multiple but not conforming to any particular pattern and were seen in 14.00%. Presence of few small discrete yellow white deposits with no visual loss; (Visual acuity 6/9 to 6/5) were seen in 7 while a faint area of depigmentation was seen with visual loss (visual acuity 6/9 to 6/12) in 5 cases. These lesions fluoresced in early phase and faded with passage of dye in choroidal circulation. Confluent drusens were seen in 24% cases and are probably a later stage in the development of disciform degeneration from scattered drusen. They are bigger in size, of different shapes and mostly associated with varying sizes of areas of pigment epithelial atrophy. These were associated with visual loss (6/18 or less) probably due to degeneration of adjoining photo-receptors. This is usually associated with patchy choroidal atrophy. In these cases we see hyperfluorescence in early phase with late staining. We, however, do not advocate any treatmet at the above two stages.
Pigment epithelial detachment (6.0%) seems to be the next stage as it was associated with either scattered or confluent drusen. It is difficult to diagnose it ophthalmoscopically but we feel that yellow gray looking area may point towards its presence. Fluorescein angiography (hyperfluorescence during early phases increasing in intensity but not in extent in consequent angiograms but always with sharply outlined margin) delineates it. Photocoagulation maybe done at this stage. It should be applied to entire area of pigment epithelial detachment if it is away from the central region (avascular region).
Subretinal neovascularisation follows changes. RPE through which choroidal new vessels proliferate and enter into subretinal space giving rise to stage IV SRNVM. Subretinal neovascularisation is the next stage as other precursor lesions may be seen. It was, however, also accompanied by certain lesions probably as an aftermath of neovascularisation.
Elevated lesion with subretinal greyish membrane, ring haemorrhage or blood alongwith peripheral edge of new vessels in subretinal space, lipid deposition with exudate like lesions, associated intraretinal haemorrhage.
New vessels or new vessel membrane arising from many points and forming a network fluoresce in the choroidal phase and start leaking from the margin in later frames on fluorescein angiography. Visual acutiy is very poor in these cases (less than 6/24 up to 6/60). Photocoagulation should be done but care must be taken about perifoveal arcade and capillary free zone of macula.
Organisation of subretinal haemorrhage into subretinal fibrovascular scar, leads to disciform lesion in the last stage with permanent to visual acuity (below 6/60 progressing to CF 1 metre). These lesions look elevated due to serous detachment of macular with intraretinal cystoid changes. Multiple intraor subretinal lipid deposition is seen peripheral to these lesions. There is marked leakage of fluorescein dye, in subretinal space (Stage V) on fluorescein angiography. The prognosis is poor as structural changes do not regress even if leakage may diminish on photocoagulation.
Disciform degeneration passes through various stages. Scattered drusen is (in and around macula) Stage I while their increase and confluent appearance ushers Stage II with effect on the visual acutiy. Appearance of pigment epithelial detachment brings about Stage III. Pigment epithelial detachment with subretinal neovascularisation (SRNV) along with subretinal and retinal haemorrhages (Stage IV) with further diminution of visual acuity. Permanent changes in the structrue (fibrovascular frond is the final stage (Stage V).
| Summary and conclusions|| |
Fellow eye is involved in 54% of the cases. Precursor lesions which progress to disciform degeneration observed in this series are drusen, either scattered or confluent, pigment epithelial detachment. Subretinal neovascularisation and haemorrhage precede classical disciform lesions. The disease has been classified into five stages. Role of fluorescein angiography in delineating precursor lesions at every stage and thereby helping in diagnosis and management of these fellow eyes is stressed. Photocoagulation of fellow eye at different stages is being evaluated to bring out exact stage and mode of therapy. Inverse relationship of senile disciform degeneration to aphakia has been observed.
| References|| |
|1.||Chandra S; Evangeloss, S.G.; Ephraim Freidman; Van Buskirk, E Michael and Klein L. Natural history of disciform degeneration of macula. 1974 Arch. Ophthalmol Vol. 78:519. |
[Table - 1], [Table - 2], [Table - 3], [Table - 4]