|Year : 1973 | Volume
| Issue : 4 | Page : 147-155
Fluorescein angiography in vascular insufficiencies
B Patnaik, S.R.K Malik, R Kalsi
Department of Ophthalmology, Maulana Azad Medical College and Associated Hospitals, New Delhi, India
Department of Ophthalmology, Maulana Azad Medical College and Associated Hospitals, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Patnaik B, Malik S, Kalsi R. Fluorescein angiography in vascular insufficiencies. Indian J Ophthalmol 1973;21:147-55
|How to cite this URL:|
Patnaik B, Malik S, Kalsi R. Fluorescein angiography in vascular insufficiencies. Indian J Ophthalmol [serial online] 1973 [cited 2020 Jun 1];21:147-55. Available from: http://www.ijo.in/text.asp?1973/21/4/147/34620
Arterial obstructions in the retina are dramatic events, specially that of central retinal artery. Complete occlusion of the central retinal artery results generally in total loss of vision. Branch arterial blocks are manifested in corresponding sector field defects with sharp borders. Very commonly there is a re-establishment of a sluggish circulation in course of time. However, if the obstruction has remained for more than a few hours, permanent visual defects persist. Following the obstruction the larger vessels are reduced to threads and smaller ones become almost invisible. The blood column in the artery often gets fragmented. The retina becomes opaque and milky white in 10 minutes to 2 to 3 hours, due to cloudy swelling of the ganglion cells. The fovea being devoid of ganglion cells stands out as a `cherry red spot'. The haziness begins to disappear after one to two days and it takes about 5 weeks for the resumption of normal appearance of the retina. The disc becomes pale. However, there could be less dramatic vascular insufficiencies of as much significance where fundus examination with an ophthalmoscope may reveal very little to help the diagnosis.
Till the advent of fluorescein retinal angiography (NOVOTNY AND ALVIS 1961) little could be known about the precise state of circulatory disturbance. Six representative cases of arterial obstructions studied by fluorescein angiography will be presented to illustrate how much this technique can help a clinician to appreciate the actual state of altered haemodynamics in cases of vascular insufficiencies.
A classical complete obstruction of central retinal artery
This 58 years old male complained of sudden painless complete loss of vision in his left eye 10 days earlier. He had no perception of light. Pupil was dilated and was not reacting to direct but reacting normally to consensual light. Media were slightly hazy because of an immature cataract. Disc was pale. Arteries were extremely thin almost thread-like. There was milky white opacity of the retina more marked in the central area with a typical `Cherry red spot' at the fovea. Electroretinography showed an extinguished pattern. (The usual procedure of bulbar massage, administration of amyl nitrate, retrobulbar priscol or duadinol did not have any effect. Administration of oral steroids on the assumption of giant cell arteritis similarly was of no avail).
Fluorescein angiography [Figure - 1]A showed a very slow filling of the branches of central retinal artery. There was a normal flush of fluorescein on the disc during a.v. phase. The fine proximal branches of both central artery and vein were seen getting filled up with the dye [Figure - 1]B. There were segmental pooling of the dye at the distal end of the blood vessels [Figure - 1]C.
The right eye was having vision of 6/12 with an immature cataract. The fundus was normal except for increased arterial reflex and sclerotic A.V. changes. The brachial blood pressure was 150/98. His arteries were sclerotic and felt hard. There was no evidence of any cardiovascular or cerebrovascular accident. Carotid pulses were normally felt on both sides. The cherry red spot in the left eye was still clearly visible 3 months after the arterial occlusion.
| Comments|| |
This seems to be a typical case of central retinal arterial block as a complication of arteriosclerosis. The obstruction of central retinal artery was presumably at the lamina cribrosa. The fine branches of central retinal vessels around the disc seem to receive fluorescein by way of ciliary artery system. Pooling of dye demonstrates poor circulation. The persistence of retinal opaqueness for over 3 months was unusual.
This 25 years old female, a case of rheumatic heart disease with mitral regurgitation, aortic stenosis and aortic regurgitation discovered a loss of lower field in the left eye on getting up from a siesta 4 days back. The anterior segments of her eyes were normal, visual acuity was 6/5 in each eye. Left eye fundus [Figure - 2]A showed an opaque retina covering the territory of the supply of upper temporal branch of central retinal artery. The artery was narrow. The blood column was segmented showing slow jerky movement [Figure - 2]B. The white plasma and red (RBC) segment were slowly moving towards the periphery. The field showed a lower nasal and partial lower temporal defect. Macula was spared.
Fluorescein angiography [Figure - 2]A showed a very slow filling of the artery with short fluorescent segments (corresponding to plasma filled segments) moving slowly and hesitatingly towards its peripheral branches. The venous return was similarly slow. The upper and lower nasal aspect of the disc was showing dye leakage indicating oedema [Figure - 2]C. The veins passing through the infarcted area were showing staining of their wall and extravasation of the dye [Figure - 2]D. Four days later the angiography showed considerable improvement in circulation [Figure - 2]E. There were 2 patches of superficial haemorrhages situated at the junction of opaque and normal retina. The field defect did sot improve.
| Comments|| |
A relatively recent case of branch arterial block clearly showing the poor circulation. The haemorrhages at the junction of infarcted to normal retina underline the pathology of red infarct. Block was presumably due to an embolus from the rheumatic heart. Upper temporal branch typically gets blocked in embolism.
This 26 years old female had sudden loss of vision in the left eye 15 days back. After a few minutes she recovered considerable amount of vision. She had an uneventful delivery one month back.
Ocular examination revealed a normal anterior segment. The lower temporal part of the retina was white opaque. The details of the blood vessel were obscured at places. The corresponding arterial branch was visibly narrow [Figure - 3]A. Her visual acuity was 6/6 in right eye and 6/12 in the left eye. The field in the left eye showed an upper nasal quadrantic loss with sharp borders [Figure - 3]B.
Fluorescein angiography: The arterial phase has been missed. The lower temporal artery has a narrow lumen. The delay in dye return in the corresponding vein is obvious [Figure - 3]C. There was also a delay in emptying of the vein.
Her systemic B.P. was 116/68. A thorough investigation conducted elsewhere did not point to any etiological factor.
| Comment|| |
The initial sudden loss of vision could be due to reflex spasm of the whole retinal arterial tree associated with the branch occlusion or may be due to embolus passing from the central retinal artery to its lower temporal branch. Except for a dubious relationship with parturition the etiology remains obscure. The partial obscuration of the large retinal blood vessels points to a retinal oedema over and above the known cloudy swelling of the ganglion cells.
This 26 years old female Santosh Saxena, had a sudden marked diminution of vision LE. 3 years back. She was treated with vasodilators elsewhere and had some improvement in vision. Again 11/2 years back she had some deterioration when she was seen in this hospital. The vision was, in RE 6/6; in LE-6/9. The field showed a typical lower nasal sectorial defect [Figure - 4]A. Since one week she had been feeling a further deterioration in the vision. A field examination revealed an extension of the defect towards the lower temporal quadrant [Figure - 4]B. The visual acuity remained unchanged.
On fundus examination the upper half of the disc looked paler. The upper temporal branch of the central retinal artery was markedly narrow. There was a suggestion of slight narrowing of the upper nasal branch. There was a little pigment mottling on the upper temporal retina. Fluorescein angiography [Figure - 4]C in the arterial phase showed a slow filling with the dye of the upper temporal and upper nasal branches. The calibre was reduced. The defective arterial flow can be estimated indirectly yet more dramatically from the delay in venous return [Figure - 4]D. The irregular patchy background fluorescence in the upper temporal quadrant indicates a disturbance of the pigment epithelium.
On this occasion an examination by the cardiologist revealed a rheumatic heart with mitral stenosis.
| Comment|| |
Vascular embolism is a known complication of mitral stenosis. Upper temporal branch is typically involved in embolism. The initial obstruction seems to be embolic. The extension to other branches could be by formation of thrombus. The obstruction being old standing and extension to upper nasal branch gradual, there was no opacity of the retina. The disturbance of the pigment epithelium could be due to late changes of vascular block.
A 44 years old woman, visited outpatients department with occasional frontal headaches. She was diagnosed as a case of glaucoma an year back and was being treated medically. Vision was 6/6 both eyes. Fundus showed [Figure - 5]A deep glaucoma type cups in both eyes. The fields showed generalised constriction to 15-200 all round in both eyes. The intraocular pressure was normal.
All tests for glaucoma were normal. X-ray skull was normal. Fluorescein angiography of left eye revealed insufficiency of the lower branch of central retinal artery [Figure - 5]B.
| Comment|| |
Vascular insufficiency of the branch retinal artery at the optic disc could be demonstrated. In the absence of any sign of glaucoma similar insufficiency in the vascular supply of the optic nerve may be presumed to explain the optic atrophy and field constriction.
This 25 years old male had sudden blurring of vision in both eyes 1½ months back. It was more marked in the right eye (RE). While the blurring cleared completely in the left eye (LE) in 36 hours there still remained a small patch of very thin veil around his fixation spot. His visual disturbance was associated with severe, throbbing headache with reeling of the head and nausea. He had three such attacks: 2 years, 1 year and 6 months back respectively. However, every time on previous occasions his vision had completely recovered within 48 hours. Sometimes his attacks of headache were not followed by blurring of vision. His visual acuity was 6/5 in each eye. The patient could outline a thin central scotoma on an Armsler's chart [Figure - 6] in the right eye. On fundus examination the foveal reflexes were slightly dull with a suggestion of a mild macular oedema. No vascular anomalies could be detected. Anterior segments were normal. Brachial blood pressure - was 120/80 mm Hg. Ophthalmodynamometry: Supine, RE-90/60; LE-85/60 Sitting:RE-85/55;LE-85/55. On fluorescein angiography [Figure - 6]A and B it was noticed that in the RE out of the pair of symmetrically placed small temporal arteries arching above and below the macula the lower one was distinctly slower in filling and emptying as compared to its upper counter part. There was no leakage of the dye in the macular area. The LE did not show any abnormality.
He was having the residual scotoma even 2 months after the fluorescein study.
| Comment|| |
Even after the fluorescein angiography, no perceptible change in arterial calibre could be detected on ophthalmoscopy. Probably the vascular obstruction was inside the disc and not visible ophthalmoscopically. It is obvious that there persisted a central scotoma and an insufficiency in arterial circulation of the lower temporal branch after the 4th attack of blurring of vision. The attacks of migrainous headache coming with the visual symptoms seem more than a coincidence. Without the aid of fluorescein angiography this vascular phenomenon would have been missed.
| Discussion|| |
Case II was a fresh case of branch arterial block, There was, however, a very slow flow of circulation, which improved markedly by the 4th day.
The leakage of the dye on the upper part of the disc and along the veins passing over the infarcted area could be due to anoxic damage to the vascular endothelium of the capillaries.
The probable causes of vascular obstruction in the first 4 cases were: arteriosclerotic thrombosis in Case I, embolic in association with mitral stenosis in Cases II and 1V, child birth (Duke Elder, 1969) in Case III.
Fluorescein angiography in these 4 cases of arterial obstruction of different duration demonstrates the approximate site, the completeness or the degree of obstruction, degree of narrowing of the lumen and the exact state of the circulation. It opens up a distinct possibility of monitoring the change in circulation as a natural phenomenon or as a response to therapy. It may be noted that even if there is a reestablishment of circulation, the retinal functions seldom reverse and the angiography can detect the defective circulation years after the block.
Case V was in all respect a case of low tension glaucoma. Vascular insufficiency at the optic nerve head has been long suspected as the cause of field defects and optic nerve atrophy in some of these cases. It has been possible to demonstrate vascular insufficiency in a retinal branch originating from the nerve head. One may reasonably assume that similar vascular changes might have affected the optic nerve head.
Simple blurring of the vision as visual phenomenon in migrain is almost universal (SELBY AND LANCE, 1960). It is believed that most of the cases of migrain in which visual obstruction alone is the chief manifestation of visual disorder are due to vasoconstriction of the retinal arteries (BEHRMAN, 1951). Occasionally such an episode is not followed by usual recovery of the vision and then ophthalmoscopy may reveal occlusion of one or more branches of central retinal artery (GRONVALL, 1938). Case VI demonstrates that even if no obstruction is seen on ophthalmoscopy in the presence of a field defect, fluorescein angiography may reveal an insufficiency. As to whether the insufficiency was due to the persistent spasm or an organic obstruction was not clear since the site of obstruction could not be visualised. It may be presumed that point of narrowing of the lumen was on or behind the lamina cribrosa.
Thus these six cases demonstrate how fluorescein angiography helped towards an understanding of the true nature of abnormal haemodynamics in various types and degrees of vascular insufficiency.
| References|| |
Behrman, S.: Arch. Ophth. 45: 458, 1951.
Duke Elder, S.: System of Ophthalmology, Vol. X. Diseases of the Retina, pp. 66, Henry Kimpton, London, 1969.
Gronvall, H.: Acta. Ophth. 16: 602, 1938.
Novotny, H. R. and Alvis, D. L.: Circulation, 24: 82-86, 1961.
Rubinstein, K. and Paton, A.: Tr. Ophth. Soc. U.K. 87: 345-354, 1967.
Selby, G. and Lance, J. W.: J. Neurol. Neurosurg. Psychiat. 25: 23, 1960.
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6]