Thrombus and branch retinal vein occlusion

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Graefe's Arch Clin Exp Ophthalmol (1997) 235:10-13 © Springer-Verlag 1997

Edoardo Baglivo

Andr6 Dosso

Constantin Pournaras

Thrombus and branch retinal vein occlusion

Received: 21 March 1996

Revised version received: 23 July 1996 Accepted: 20 August 1996

E. Baglivo ( ~ ) • A. Dosso • C. Pournaras Clinique d'Ophtalmologie,

H6pital Cantonal Universitaire, Rue Alcide-Jentzer, 22, CH- 1205 Geneva, Switzerland Tel. +41-22-38.26.429; fax +41-22-382.83.82; e-mail baglivo-edoardo @ diogenes.hcuge.ch

Abstract

B r a n c h retinal vein occlusion ( B R V O ) is often a s s o c i a t e d with arteriosclerosis. T y p i c a l l y the o c c l u s i o n o c c u r s at an arteriovenous crossing. We r e p o r t a case o f a p r e v i o u s l y h e a l t h y patient w h o d e v e l o p e d a B R V O . F u n d u s c o p y and f l u o r e s c e i n a n g i o g r a p h y suggested an intravascular t h r o m b u s as the cause o f the occlusion. T h e investigations p e r f o r m e d were posi- tive for systemic h y p e r t e n s i o n and

h y p e r l i p i d a e m i a . A f t e r 2 months, f u n d u s e x a m i n a t i o n revealed dis- a p p e a r a n c e o f the intravascular t h r o m b u s , resolution o f the m a c u l a r e d e m a and i m p r o v e m e n t o f the - visual acuity. C e r t a i n physiological characteristics o f the retinal circulation a s s o c i a t e d with h y p e r l i p i - d a e m i a and systemic h y p e r t e n s i o n a p p e a r to favour t h r o m b u s f o r m a - tion.

Introduction

Case report

A c u t e b r a n c h retinal vein o c c l u s i o n ( B R V O ) presents a characteristic clinical picture with f l a m e - s h a p e d and dot and blot h a e m o r r h a g e s , soft and hard exudates, retinal o e d e m a and a dilated vein in a s e g m e n t a l distribution. T h e o c c l u s i o n invariably appears to o c c u r at an arteriovenous (AV) c r o s s i n g point [9, 10]; t h i c k e n i n g o f the arterial wall and the p r e s e n c e o f a c o m m o n adventitia o f the a r t e r y and the vein at AV c r o s s i n g s s e e m to play a role in the p a t h o g e n e s i s o f the B R V O [10, 16],

T h e m a j o r risk f a c t o r is arteriosclerosis (age, systemic h y p e r t e n s i o n , diabetes mellitus, s m o k i n g , h y p e r l i p i - daemia). O t h e r p r e d i s p o s i n g factors, such as blood dyscrasias, l y m p h o - p r o l i f e r a t i v e disorders, periphlebitis (sarcoidosis, B e h c e t ' s disease, retinal infections), h y p e r - opia and o p e n - a n g l e g l a u c o m a have b e e n d e s c r i b e d [ 1 - 3 , 12, 15, 17].

We r e p o r t here the case o f a 5 3 - y e a r - o l d m a n w h o developed an o c c l u s i o n o f the superior t e m p o r a l vein. F u n d u s c o p y and f l u o r e s c e i n a n g i o g r a p h y o f the o c c l u - sion s u g g e s t e d the p r e s e n c e o f an intravascular t h r o m - bus.

A 53-year-old previously healthy man presented in December 1992 with a 2-day history of sudden decrease of visual acuity in his left eye.

On examination, the patient's visual acuity for distance was 10/10 with -0.75 in the right eye, and the best corrected visual acuity in the left eye was 5/10. Intraocular pressure was 10 mmHg in both eyes. Results of slit-lamp examination were normal in each eye. Fundus examination of the right eye showed minimal arteriosclerosis. In the left eye, a superotemporal BRVO was noted. Whitish intravascular material was observed in a segment of the occluded vein at two disc diameters from the optic disc (Fig. 1). The fluorescein angiography showed staining of the venous wall at distance of the proximal end of the intravascular material. The hyperfluorescence was visible in the early arteriovenous phase and increased in the mid-phase of the angiogram. Distal to the intravascular material, the retinal venous circulation time was increased (Fig. 2a). At the site of the venous occlusion, the biomicroscopic and angiographic findings suggested that this material was an intravascular thrombus. Moreover, in this area, a breakdown of the blood-retinal barrier was observed (Fig. 2b).

We performed investigations for systemic hypertension, diabetes mellitus, hyperlipidaemia, connective tissue disorder, Be- hcet's disease, sarcoidosis and blood dyscrasia. Results were posi- tive for systemic hypertension and hyperlidaemia [HDL cholesterol 0.52 retool/1 (n = 0.75-1.73); total cholesterol 8.03 retool/1 (n = 3.3-6.5); LDL cholesterol 4.81 mmol/1 (n = less than 3.9);

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II

Fig. 1 Left fundus photograph. The superotemporal vein, distal to the whitish intravascular material occluding the venous lumen, seems dilated. Hard exudates and retinal h a e m o r r h a g e s are local- ized in the affected retinal area

Fig. 2a, b Mid-arteriovenous phase fluorescein angiogram, a De- layed filling of the superotemporal vein distal to the occluded venous segment; b staining of the venous walls at the site of occlusion and persistence of a narrow lumen stained by the dye Fig. 3 Left fundus photograph. Two months later, the thrombus has disappeared. A narrowing of the venous diameter at the site of the thrombus can be observed

Fig. 4 M i d - p h a s e fluorescein angiogram. The thrombus and the delayed filling of the superotemporal vein are no longer apparent

triglycerides 5.94 mmol/1 (n = 0.4-1.83)]. We excluded sec- ondary dyslipidaemia (hypothyroidism, diabetes, liver disease, re- nal disease). The patient did not drink alcohol, did not smoke and was neither obese nor a drug abuser.The systemic h y p e r t e n s i o n was treated with a calcium channel blocker and the dyslipidaemia

with hypolipaemic medication (benzylfibrate), and we introduced salicylates (100 rag/day). Dietary advice was given.

Two days later, the visual acuity of the left eye had worsened ( 3 / 1 0 ) and retinal examination showed macular oedema. Due to the persistence of the macular o e d e m a and the presence of is-

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chaemic areas, argon laser photocoagulation was performed 6 weeks after the diagnosis.

Two months later, the visual acuity of the left eye had improved (10/10 without correction). Fundus examination showed the disappearance of the whitish intravascular material and a resolution of the macular oedema (Fig. 3). Fluorescein angiography revealed reperfusion of the superior temporal vein (Fig. 4). Finally, the lipidogram and the patient's blood pressure were normal.

Discussion

Leber [14] was the first to suggest the importance of arteriosclerosis and the vulnerability of AV crossing sites in BRVO. Jensen observed that the artery lay anteri- or to the vein at the majority of BRVO crossing sites and postulated that the predilection of BRVO for the superotemporal quadrant was due to the greater number of crossings in this quadrant [ 11 ]. Others have recently con- firmed Jensen's observation of a greater percentage of artery-anterior-to-vein crossings at the BRVO sites [7, 19] and of a greater number of crossings in the superotemporal quadrant [8]. A histopathologic study con- firmed the importance of the AV crossing at the site of the BRVO [10]. In our case, we observed, at the site of the occlusion, an intravascular white material occluding the vessel's lumen without any sign of ocular inflamma- tion. This material disappeared two months later.

These observations suggest that the cause of the occlusion was the presence of a thrombus. The follow-up was characterized by the disappearance of the thrombus

and the recanalisation of the superotemporal vein. As risk factors, our patient had high blood pressure and hyperlidaemia. This seems to be the first clinical report of a BRVO caused by a thrombus.

Since the F r a m i n g h a m study [13], hyperlidaemia as an isolated predisposing factor furthering atherosclero- sis in large vessels or an ischaemic arterial stroke has been well documented [18]. Nevertheless, few studies describe venous thrombosis occurring in association with dyslipidaemia [4].

Dodson and colleagues [5, 6] found a greater prevalence of hyperlipidaemia and hypercholesterolaemia in patients suffering from BRVO than in an age-matched group. They proposed that the increase of serum lipids may contribute to the aetiology of vein occlusion by al- tering plasma viscosity or affecting platelet function.

There is general agreement that the origin of BRVO includes both systemic factors such as hypertension and local anatomical factors such as AV crossings. However, the initial p h e n o m e n o n causing such condition is still uncertain.

In our case, the mechanical factor was absent. Whether the thrombus formation was due to abnormal blood viscosity or alteration of platelet function, induced by hyperlipidaemia, could not be ascertained. However, it appears that hyperlipidaemia and hypertension may favour intravenous thrombus formation, and the treat- ment of risk factors seems to improve the natural course of the disease.

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