Year : 1979 | Volume
: 27 | Issue : 4 | Page : 166--169
Retinal function in branch vein obstruction
Bijayananda Patnaik, Rajinder Kalsi, Madan Deshpande, Noshir Shroff
Maulana Azad Medical College, New Delhi, India
Maulana Azad Medical College, New Delhi-110002
|How to cite this article:|
Patnaik B, Kalsi R, Deshpande M, Shroff N. Retinal function in branch vein obstruction.Indian J Ophthalmol 1979;27:166-169
|How to cite this URL:|
Patnaik B, Kalsi R, Deshpande M, Shroff N. Retinal function in branch vein obstruction. Indian J Ophthalmol [serial online] 1979 [cited 2021 Jun 20 ];27:166-169
Available from: https://www.ijo.in/text.asp?1979/27/4/166/32616
Various forms of field defects have been described in branch retinal vein obstruction. The widely described changes are: sector shaped defects in the corresponding quadrant, central and paracentral scotomas. Lately emphasis have been laid on arcuate type or sector shaped defects, considered to have been caused by associated arterial insufficiency,.
Since the introduction of the principle of multiple spot photocoagulation to convert the hypoxic areas to anoxic scars in way of preventing growth of new vessels (Diabetic Retinopathy study Research Group, 1976) and the application of this principle in management of branch vein obstruction, it has become important to assess the state of function of the affected retina to be treated by destructive photocoagulation. This study presents findings of kinetic and static perimetry in brahch vein obstruction of both inflammatory and sclerotic nature.
Materials and Methods
Fifteen patients of fluorescein angiography clinic of Retina Care Department of this institution with branch vein obstruction were studied by kinetic and static perimetry using a Goldmann projection perimeter. There were 11 of inflammatory and 4 of arterio-sclerotic etiology. Six had single branch obstruction and 9 showed involvement of Multiple venous branches. Incidentally all these cases were males with age varying from 20 years to 60 years. All the cases of venous obstruction due to arteriosclerosis were of 5th decade. All but 2 cases of inflammatory etiology were of 2nd or 3rd decade. The remaining 2 were of 4th decade.
The method of correlating fundus and field
The Goldmann projection perimeter charts and the charts for fundus drawings, are comparable in size. A system was evolved of direct correlation by approximation by taking into consideration of following plants:
1. The image (therefore the field) is actually formed inverted on the fundus.
2. The visual field is what patient sees and therefore has to be viewed by the examiner `from the patient' along his line of vision. On the other hand the fundus is visualised and charted by the examiner while he is looking towards the patient.
Testing the accuracy of the method of correlation required indentifying points just inside and outside the retinal territory affected by venous obstruction on applying isolated photocoagulation spots at predetermined points and identifying them on the visual field.
When a fundus diagram was drawn using an indirect ophthalmoscope, where vascular branching are shown at proportionate distances from the disc, keeping disc and ora as reference points, the direct correlationship between the fundus drawings and Goldmann field charts were remarkably satisfactory [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5]. On the basis of fundus picture [Figure 1] B photocoagulation marks could be placed and identified at the predictable situations in the field [Figure 1], circle of dots with hatched lines).
Arterio-sclerotic branch vein obstructions produce milder and more localised field defects [Figure 2],[Figure 3]. The visual disturbance was more serious in fresh cases (6/36: 15 days: B.N.M. [Figure 3]). The vision improves with time (6/9: 4 months: C•D.S. [Figure 2]) often a paracentral [Figure 2] occasionally a central scotcma may persist specially when upper temporal vein is involved. Prompt use of anticoagulants improves circulation, reduces and macular oedema and improves both visual acuity (6/36 to 6/12: [Figure 3] and visual fields [Figure 3]. Identification and delineation of a small central or paracentral scotoma is difficult by kinetic perimetry. Thus the centro-coecal scotoma missed in kinetic perimetry can be clearly demonstrated by static perimetry (profile perimetry) as shown in [Figure 2].
On the other hand the field loss in inflammatory venous obstruction is both gross and permanent in the affected sector [Figure 4] and 5). Initially the central vision is affected 6/36: 4 weeks: J.N. [Figure 4]). In due course the central vision m.ty improve. However persistence of ishaemia with hypoxia seem to cause generalised depression of the peripheral isopters. The same factors also stimulate neovascularisation- Multiple spot coagulation over the affected area improve the field [Figure 5]: compare [Figure 4]. isopter on 2.11.1976 with that on 15.11.1976-just before and 2 weeks after photocoagulation).
The peripheral field loss due to branch vein obstructions conforms well to the area of involvement. In general the arterio-sclerotic obstructions are associated with milder defects with slopping borders. There is a tendecy for improvement with time or with treatment. The process of compensation through development of collateral communication recanalisation is more complete. The development of neovascularisation is therefore less common. This could be due to the fact that the process of obstruction is slow, permitting enough time for circulatory adjustment. Besides, the obstruction is rarely complete.
On the other hand the venous occlusion due to phlebitis is rapid and often complete. The field defects are gross and the border of the field in the defective quadrant is steep. There is little tendency for recovery. Even when the fundus picture assumes a near normal look with only occasional colleteral vessels or kinks to indicate past involvement, the field loss continues to be gross. Besides, the spread of inflammation to smaller branches may be contributing towards the total occlusive process.
None of the cases in this series have shown arcuate field defects attributable to arterial insufficiency as claimed by some,.
The attenuation of arterioles, at least, in inflammatory venous obstruction have been shown in a series of follow up studied to be secondary to venous obstruction.
The generalised depression of isopters in branch vein obstruction is interesting. Improvement of circulation following the use of anticoagulants or reduction of areas of hypoxia by multiple spot coagulation leads to expansion of depressed isopters. This may lend support to the belief that regional ischaemia or hypoxia of the retina has a toxic or deleterious effect on the entire retinal function.
Central or paracentral scotomas are more frequent than believed. Being small or relative they are difficult to detect by kinetic perimetry. However, static perimetry carried out in various meridians would detect them with accuracy. The precise cause of their development is not clear.
Since inflammatory branch venous obstruction often lead to neovascularisation-specially when areas of capillary non-perfusion can be demonstrated by fluorescence photography, and multiple spot photocoagulaiion seems to be helpful in preventing their development, the state of function of the retina to be photocoagulated should be ur.derstcod. A field examination, particularly of the affected sector is indicated. However, broadly speaking one could expect a field loss conforming to the area affected, specially when affected region show areas of capillary non-perfusion.
After confirmation by a field examination one could photocoagulate the affected sector aiming at destroying the greater part of hypoxic retina.
Kinetic and static perimetry in branch retinal vein obstruction in sixteen cases shows that the peripheral field defects conforms very well to the retinal area involved. The field defects in inflammatory vein obstruction are more profound as compared to arteriosclerotic ones. Detection of small central or paracentral scotoma so often present, are easier with static (profile) perimetry, than on the kinetic perimetry.
|1||Aulhorn, E., 1963, Klin. Monatahl. Augeneilkd., 143, 234.|
|2||Birchall, C.H., Harris, G.S., Drance, S.M. and Beg, I.S. 1976, Arch. Ophthal., 94, 747.|
|3||Patnaik, B., Kalsi, R. and neshpande, M., 1977, Presented at XXXVI All India Ophthalmological Conference.|