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ARTICLES |
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| Year : 1983 | Volume
: 31
| Issue : 3 | Page : 176-178 |
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Sub-retinal neo-vascularisation
Chandran Abraham, SS Badrinath
Sankara Nethralaya, Medical Research Foundation, 18 College Road, Madras-6, India
Correspondence Address:
Chandran Abraham
Sankara Nethralaya, Medical Research Foundation, 18 College Road, Madras-6
India
PMID: 6202630
How to cite this article:
Abraham C, Badrinath S S. Sub-retinal neo-vascularisation. Indian J Ophthalmol 1983;31:176-8 |
Subretinal Neovascularisation (SRNV) is a clinical entity that has been recognised after the utilisation of fluorescein angiography in the study of chorioretinal diseases. The neovascularisation is from the chorio-capillaries which proliferate through a break in Bruch's membrane to beneath the retinal pigment epithelium. In this situation they can cause a retinal pigment epithelial detachment. They can also proliferate through the pigment epithelium to lie beneath the sensory retina causing a sensory retinal detachment. Subretinal neovascularisation can be idiopathic or associated with a variety of conditions. Central vision can be permanently impaired if subretinal neovascularisation invades the fovea. Left untreated they result in the formation of haemorrhages, exudates and fibrous tissue-the picture of a disciform macular degeneration. However, the natural history of this disease can be varied. The management consists of early recognition of this entity by fluorescein angiography, meticulous treatment by photocoagulation in selected cases and careful follow up.
 Materials and Methods | |  |
28 eyes of 25 patients with subretinal neovascularisation seen at Sankara Nethralaya between June 1979 and June 1981 forms the basis of this study. 17 were males and 8 females. The youngest was 27 years and the oldest 78 years of age. Clinical examination consisted of recording the best corrected visual acuity for near and distance, indirect ophthalmoscopy, colour photography and fluorescein angiography of the fundus, Amsler charting and recording of colour vision was done in most of the cases. Argon Laser photocoagun lation was performed in 6 eyes and the Xenon arc in 3. A recent negative of the fluorescein angiogram showing the extent of the net in the arterio-venous phase was projected during the treatment. The fovea was always identified prior to commencement of treatment. Fluorescein ophthalmoscopy was also done in certain situations. A retrobulbar block was administered to most patients treated with the Laser and to all those treated with the Xenon. Heavy confluent coagulations using a spot size of 200 or 100 micron with a timing of 0.05 to 0.2 seconds were applied to the entire lesion after marking the foveal border of the lesion with a row of 50 micron burns. The 1.5 spot size was used while using the Xenon arc photocoagulator, the exposure time was set at 0.2; 0.3 or 0.5 seconds and the power adjusted to produce the desired heavy coagulations, The criterion for treatment was threat to foveal vision, Lesions which had invaded the fovea or were situated 300 micron or closer to the fovea were not treated. Treated patients were seen the next day and then after a week when colour photography and fluorescein angic. graphy were repeated. Patients who showed persistance of the lesion were re-treated. They were then seen after 3 months. 3 treated eyes have been followed up for more than 6 months, 3 between 2 and 6 months and the remaining for a month. 5 untreated eyes have been followed up for more than 6 months and 7 for a period between I and 6 months.
Clinical features:
Most patients (22) presented with complaints of reduced visual acuity. 8 complained of metamorphopsia, 7 of scotoma., 2 of micropsia and I of diplopia. The duration of these symptoms was varied. Amsler charting showed 5 to have metamorphopsia, and 12 to have scotomas. While there was no consistent corelation between the patients' visual acuity and the findings in the macula and foveal invasion by subretinal neovascularisation, most of the patients where the fixation spot was involved as shown by Amsler charting had foveal involvement. Ophthalmoscopically subretinal neovascularisation presented as a central serous retinopathy in 11 eyes, senile disciform degeneration in 12 and as a Fuch's spot in 2. There was associated angioid streaks in 1, choroidal inflammation in 1, and in another subretinal neovascularisation had developed from a heavy xenon photocoagulation scar used to treat a central serous retinopathy. A careful examination revealed a dirty white or yellow membrane in the region of macula in 6 eyes. It was impossible to delineate the sub retinal neovascularisation on ophthalmoscopy alone. Fluorescein angiography was diagnostic in all cases. It showed typical early lacy hyper fluorescence in 13 eyes. The fluorescence was nodular or irregular in 1(). 3 eyes showed features of a leak as in central serous retinopathy.
A cartwheel pattern of hyperfluorescence was made out in 2 eyes and in another 2 it presented as a retinal pigment epithelial detachment, one of which showed a hot-spot within. 10 fellow eyes were normal on ophthalmoscopic examination. 5 showed whitish rounded lesions, 2 had senile macular degeneration, 2 drusen, and another 2 had central serous retinopathy.
Fluorescein angiography showed 4 fellow eyes to be normal. Retinal pigment epithelial defect were present in 6, subretinal neovascularisation in 4 and central serous retionpathy in 1.
| Results | | |
There was complete destruction of the sub-retinal neovascularisation in 7 eyes that were photocoagulated. The associated sensory retinal detachment settled rapidly. SRNV persisted in 1 while in another it progressed. The visual acuity had improved in 3, was maintained in 3 and deteriorated in 3. There was a bleed deep to the retina during photocoagulation in 1. This involved the fovea and was responsible for the drop in vision. In I eye vision deteriorated due to progression of subretinal neovascularisation and in another who did well, we are unable to account for the deterioration. 4 eyes showed improvement when tested with the Amsler chart. It was unaltered in I while 3 showed worsening. Colour vision had improved in 3, remained unaltered in 5 and worsened in 1.
The visual acuity in 9 untreated eyes was maintained. While none improved, 3 deteriorated. Amsler charting showed worsening in 3 while colour vision was maintained in 3. Fluorescein angiography showed no progression of the lesion in 3 eyes while a regression was observed in 1.
| Discussion | | |
Fluorescein angiography is indispensable in the management of subretinal neovascularisation. It is not only diagnostic but also aids in deciding whether to treat a patient or not. The adequacy of photocoagulation can be judged only by fluorescein angiography. Photocoagulation seems to have a definite role in treating subretinal neovascularisation. It not only destroys the lesion and prevents its spread to the fovea but also helps in resolution of the accompanying sensory retinal detachment, blood and exudates. As inadequate photocoagulation acts as a stimulus to progression of subretinal neovascularisation, treatment should be complete, as described. The most important factor is the decision to photocoagulate or not. Once we decide to treat we should treat adequately. The best chance of attaining success in treatment is the first session of photocoagulation. Dangers of foveal damage and damage to the nerve fibre layer should be constantly borne in mind and the risk-benefit ratio carefully evaluated before embarking on treatment. Our visual results are quite gratifying. We believe that treatment was responsible for the improvement in vision in 3. The 3 eyes maintained vision without treatment. In only 1 eye was photocoagulation directly responsible for the reduction in vision. The 9 untreated eyes which maintained the same vision, were eyes where the fovea was already involved. 3 had deteriorated further. Improvement in Amsler charting in 4 treated eyes is also significant as patients are quite troubled by scotomas and metamorphopsia. The worsening in 2 is most likely due to photocoagulation while in another, progression of subretinal neovascularisation. It is quite interesting to note that repeat angiogram in untreated eyes showed no progression in 3 and regression in 1. These eyes will be followed up periodically to see how the natural course of the disease runs. In our limited experience of using both the Laser and the Xenon in dealing with subretinal neovascularisation, we feel both are as good. The disadvantages of the Xenon are however serious and are as follows:
i) With the minimal settings possible on the machine, one could still get an undesirably heavy burn.
ii) The field of view is so small particularly when choosing the smallest aperture of 1.5° and this makes foveal identification extremely difficult. It is also difficult to judge distances from the fovea and corelate land-marks seen on the angiogram. Thus good experience and considerable skill are needed to deal with this situation.
| Summary | | |
The ophthalmoscopic and fluorescein angiographic features of subretinal neovascularisation in 28 eyes of 25 patients are described. The technique of Argon Laser and Xenon arc photocoagulations, the results of treatment, the role of fluorescein angiography and photocoagulation in the management of subretinal neovascularisation are discussed.
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