|Year : 1958 | Volume
| Issue : 1 | Page : 1-4
Central retinal vein thrombosis. Report of a case treated with tromexan
|Date of Web Publication||8-May-2008|
E J Somerset
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Somerset E J. Central retinal vein thrombosis. Report of a case treated with tromexan. Indian J Ophthalmol 1958;6:1-4
|How to cite this URL:|
Somerset E J. Central retinal vein thrombosis. Report of a case treated with tromexan. Indian J Ophthalmol [serial online] 1958 [cited 2020 Apr 8];6:1-4. Available from: http://www.ijo.in/text.asp?1958/6/1/1/40711
Central vein thrombosis is, of course, a relatively common condition, well-known to all ophthalmologists. First described by Julius V. Michael in 1878 much has been written on the subject since then but even so, many points in the aetiology and in the intimate mechanism are still unknown Duke-Elder (1940) suggests that the mechanism of occlusion is as follows; there is a pre-disposing slowing of the blood flow. Occasionally this may be associated with toxic or marasmic states, or associated with sclerotic disease which may occur as a general or as a mainly local condition. The retinal arteries and veins are intimately connected with each other at the arterio-venous crossings on the retina and at the level of the lamina cribrosa, where they may have a common intervening wall. Any sclerosing pathological process affecting the artery will therefore readily spread to the vein. Thrombosis, therefore, tends to occur at both these sites. Another small point is that the central vein sometimes leaves the nerve about 2 mm. behind the globe instead of the usual 7-15 mm. The blood stream will therefore negotiate two sharp right-angled bends in these cases instead of a relatively easy and gradual curve.
The second factor in the mechanism is the formation of a roughened area on the endothelium upon which deposits may collect. Upon this area cells and fibrin may be deposited from the relatively stagnant blood so that a nodule of organised thrombosis protrudes into the lumen of the vein. Alternately, some consider that it is more likely that in most cases there is an endophlebitis with proliferation of the endothelium, which similarly gradually fills the lumen. Lastly this may lead to total occlusion of the vein and thrombosis. It is interesting to note that Ennema & Zeeman (1953) examined 4 cases of central vein thrombosis in which subsequent enucleation for glaucoma became necessary. In 2 cases serial sections of the optic nerve revealed a clot within the lumen of the central vein but in 2 others the vein lumen was empty and obliterated or narrowed by sclerosis. In all cases the central retinal artery showed gross sclerosis.
Clinically, when the retinal vein gets thrombosed, there is a sudden loss of vision of the eye. Examination reveals enormously dilated and tortuous retinal veins, oedema of the disc and macula and multiple scattered haemorrhages throughout the fundus, particularly dense along the course of the veins.
Subsequently the circulation is restored by canalisation of the clot and by opening up of communications with adjoining veins through the capillaries. These new vessels may sometimes subsequently be seen on the disc. Glaucoma supervenes in some 10-20% of cases during the next 3 months.
In most cases vision which has been suddenly reduced to counting fingers at a few feet, deteriorates inspite of the restoration of the venous drainage and absorption of the haemorrhages. The prognosis for vision is not good, Duke-Elder (1940) however notes that "very rarely the circulation is restored within a few weeks, and such exceptions are probably the foundation for over-optimistic claims which have been made for heparin and other drugs employed in the treatment of this condition". Huggett and Juler (1942) in a follow-up of 32 cases of central vein thrombosis found improvement of vision in only 6 while 26 failed to recover even 6/60 vision. The recovery of vision in the more fortunate cases takes many months.
The course of thrombosis of the retinal veins is discussed in an interesting paper by Lister and Zwink (1953), I hey note the extrordinary variety of anatomical end results, and classify them into 4 groups :-
(1) Cases which show apparent complete recovery, both anatomical and functional, with minimal new vessel formation.
(2) Cases in which an obvious venous by-pass forms at the disc with great restoration of vision (6/12).
(3) Permanent damage is greater with gross vascular change such as new vessel formation, narrowing and sheathing of the veins and retinitis proliferans and vision of about 1/60.
(4) Cases showing gross change in the vitreous, gross loss of vision and sometimes retinal detachment.
They note further that functional recovery depends on the extent of damage to the macula. Of 12 cases of central vein thrombosis 4 achieved 6/12 or better (but let it be noted, only one of the four had initial vision as bad as 6/36). They think that "as a rule the final vision is approximately the same as that at the outset but that there are exceptions, some of which recover well after a bad beginning while others show progressive deterioration".
The value of anti-coagulant therapy in these cases cannot yet be finally assessed. Lister and Zwink (1953) used tromexan in a small series of cases but found no good results, in fact a number continued to deteriorate while under treatment. Adverse results are also recorded. Most of those who have published their results declare that there is no improvement; (Wessely, 1948; Rosengran, 1950; Cantallera, 1951). King (1953) noted a case of branch thrombosis which developed rapid extension of the thrombosis while under treatment with heparin, and Jensen (1950) saw a case of central vein thrombosis occur while the patient was being treated with dicoumarol for coronary 'thrombosis.
On the other hand Palomar (1947) recorded the use of heparin in 1941 in 4 cases with improvement in 3 and therapy with dicoumarol in 8 cases with improvement in 6. Favourable results with heparin and dicoumarol were also recorded by Pagliarani (1949). Beneficial results were noted by Gaspari (1952), Doren° (1953) and Santos et al (1953) in cases of retinal thrombosis treated with tromexan and with heparin by Bourde (1953) and Sedan (1953).
| Illustrative Case|| |
S. B. B., age 55, Indian clerk, complained that about midday on l0th June, 1957 he noticed sudden loss of vision of the left eye. Early the next morning he went to a hospital where central vein thrombosis was diagnosed and vision recorded as counts fingers at ½ metre. His blood pressure was recorded as 145/90 and he was directed to the X-Ray and Ear, Nose and Throat departments for further investigation. He went to his office and was sent to me later that same morning and I found as follows :-
Left Eye - Vision, counts fingers at 2 feet. Refraction about +0.50 D hypermetropia. Fundus showed that all branches of the central retinal vein were much engorged, the whole fundus was bespattered with haemorrhages mostly in the nerve fibre layer and particularly concentrated along the branches of the veins. The heaviest concentrations were along the upper and lower nasal branches but there were a large number along both temporal branches as well. There was slight oedema of the disc and macula but no visible haemorrhage at the fovea. The picture was typical of a recent central vein occlusion.
Right Eye - Vision 6/6. The fundus vessels showed slight signs of arterio-sclerosis with slight overall narrowing of the arteries. There were a few drusen in the macular area.
There was no significant history of ill health. He was edenturous and blood pressure (on 16-7-57) was 130/70. The radial and superficial temporal arteries were considerably thickened and felt sclerotic. Heart and lungs were normal and spleen and liver were not palpable. No focus of sepsis was found. The urine contained no albumin or sugar. Blood count (9-7-'57) RBC 3,490,000, WBC. 4400, Hb. 71%, Polymorphs 52%, Lymphocytes 40%, Monocytes 2%, Eosinophils 6%.
He was given Ethylbiscoumacetate BP.o.3 gram (Tromexan one tablet) at about 1.0 p.m.(about 24hours after the onset of symptoms) and another at 6 p.m. and then tablet twice daily. Slight improvement of the vision was noted 2 days later but 4 days after commencing treatment vision had improved to 6/6o and there was less engorgement of the veins. Prothrombin time was 25 seconds so he continued to take tromexan tablet twice daily and 3 days later vision had improved to 6/18 (partly). Vision on the eleventh day was still 6/18 (partly) but as the prothrombin time was now 65 seconds the drug was discontinued for 4 days after which prothrombin time was 19 seconds and the tromexan was resumed at the same dosage. Meanwhile vision had improved to 6/12, prothrombin time was 3o seconds arid the dose was reduced to 1/4 tablet twice daily. Vision continued to improve to 6/9 a few days later. The calibre of the veins was now about normal and many of the haemorrhages had absorbed(25 th day).As the prothrombin time was 44 seconds the tromexan was discontinued on 9th July (28th day of treatment).
The blind spot in the left eye is of normal size and no scotoma to the 3/1000 white target could be found. (16th July, 1957) By the 25th July 6 weeks after the onset, only a very few scattered haemorrhages could be found on careful search. They could be seen, however, in relation to all four branches of the central vein.
| Discussion|| |
Perusal of the literature has shown that prognosis in central vein thrombosis is by no means hopeless and that a small proportion of cases regain vision without treatment. Nevertheless the original vision of counting fingers at 2 feet, 24 hours after the onset, in the case reported, shows that the condition was severe and clinical examination revealed involvement of all the branches of the central vein. Visual improvement to 6/18 in 7 days is remarkable, especially in view of the severity of the original loss. For this reason one is tempted to feel that the tromexan therapy may have been beneficial. However it will require a large series of cases similarly treated before one can compare the results with earlier series.
| Summary|| |
A case of central retinal vein thrombosis with vision of counting fingers at 2 feet 24 hours after the onset of symptoms improved to 6/18 in 7 days and subsequently to 6/9 after 3 weeks. Absorption of haemorrhages was rapid. Some general sclerosis of the larger arteries was apparent though evidence of this in the fundus oculi was slight. Possibly tromexan therapy may have been beneficial and trial in a large series of cases is indicated.
| References|| |
Bourde C., (1953) Marseille Med. 90, 342.
Cantallera J. A., (1951) Arch. Soc. oftal. Hispano-Amer. II, 373.
Doggart, J. H., (1949) "Ophthalmic Medicine" Churchill, London, p. 167.
Dorello, U., (1935) Rass. et al. oftal. 22, 286.
Duke-Elder, Sir, W. S., (1940) "Text-book , of Ophthalmology", Kimpton, London, Vol. III, p. 2578.
Ennema, M. C., and Zeeman, W. P. C., (1953), Ophthalmologica (Basel), 126, 329.
Gasparri, F., (1952), G. et al. 5, 397.
Huggett, A., St. G., and Juler, F. A., (1942), Trans. Ophthal. Soc. U. K. 62, 123.
Jensen, J. P., (195o), Nord. Med. 43, 996. U. K., 73, 71.
King, E. F., (1953), Trans. Ophthal Soc., Lister, A. and Zwink, F. B., (1953), Trans. Ophthal. Soc., U. K., 73, 55.
Lyle, T. K., and Cross, A. G., (1954), May and Worth's "Manual of Diseases of the Eye", IIth edition, Bailliere, Tindall and Co., London, p. 307.
Pagliarani, N., (1949), Gior. Ital. Oftal. 2, 335.
Palomar, A. P.,(1947), Arch. Soc. Oftal Hisp-Amer. 7, 263.
Rosengren, B.,(1950), Nord. Med. 44.2882.
Santos, R. H. G., Castro, C. M. and Stritzler, G.,(1955), Arch. Oftal. B Aires, 30, 149.
Sedan, J.,(1953), Sud. Med. Chir. 86, 2824.
Wessely, K.,(1948), Ber. Deutsch Ophthal. Ges. Heidelberg. 54, 24.