Jon Bourton shows us another case study from the Institute of Optometry, a somewhat unusual presentation of a familiar condition
A Caucasian male aged 68 attended for an eye examination due to a sudden and rapid reduction in visual acuities, first noticed two weeks previously. The patient reported that he woke one morning to find he was unable to read the newspaper even with his reading spectacles and from that point on he had noticed a bilateral reduction in both his distance and near visual acuities. Visions were: 6/60 in the right eye and 6/60 in the left eye.
Subjective finding:
R +4.00/ -0.75 x 108 VA 6/9-2 ADD +2.25 N6
L +5.00/ -1.00 x 110 VA 6/12 ADD +2.25 N6 (No improvement with pin hole R or L)
High blood pressure had been diagnosed in September 2004. Following pupil dilation, indirect ophthalmoscopy revealed bilateral branch retinal vein occlusions. In the right eye there was an inferior branch retinal vein occlusion (BRVO) with numerous intraretinal haemorrhages (flame shaped) in an arcuate pattern extending three disc diameters horizontally and vertically and two disc diameters inferiorly to the disc temporally (Figure 1a). Within the central region of haemorrhaging, exudates were observed. In the left eye a superior branch retinal vein occlusion was observed with flame shaped haemorrhaging one disc diameter superiorly/temporally to disc and two disc diameters both vertically and horizontally in size (Figure 1b).
No cotton wool spots or neovascularisation was seen. Hypertensive and atherosclerotic changes were present with nipping at the majority of arteriovenous (A/V) crossings, an A/V ratio of 1/2 to 2/3 and colouration changes of the artery reflex.
Visual field examination found a defect in the left superior quadrant and small defects in the right superior and inferior quadrants. In the left eye all four quadrants showed defects of variable degrees (Figure 2).
There were no other symptoms and except for some co-existing mild irritation/discomfort associated with poor lid hygiene and mild blepharitis and very early bilateral nuclear cataract all other findings were within normal limits.
Arterial compression of the vein is believed to be the main cause of BRVO.1 When a vein is compressed by an overlying artery (the artery is anterior to the vein), the flow of blood passing that point is changed and can lead to increased turbulence. The turbulent flow of blood in combination with pre-existing endothelial vascular damage creates a local environment favourable to intravascular thrombus formation. Conditions, which can lead to retinal endothelial vascular damage, are hypertension, atherosclerosis, inflammatory, or thrombophilic conditions.
BRVO tend to occur in the supertemporal quadrant, which may be related to the increased number of arteriovenous crossings in this quadrant compared to the rest of the retinal fundus. No race or sex predilection for the disease has been recorded; however, a patient's age may be a factor as BRVO usually affect patients in their fifth or sixth decades of life. A population-based study from Australia, the Blue Mountain Eye Study found the prevalence of BRVO in the population older than 48 years to be 1.1 per cent.2
Despite the strong association of hypertensive retinopathy and hypertension, according to van den Born, the link between hypertensive retinopathy and blood pressure is low and there is little evidence that routine direct ophthalmoscopy is of additional value in the management of hypertensive patients.3 However, other studies,4 while stressing the multifactorial character of systemic hypertension, claim that fundus changes are directly related to the control of blood pressure and that direct ophthalmoscopy is the best tool to identify these changes. It has also been claimed5 that hypertensive retinal microvascular changes increase the chance of coronary heart disease (CHD) by twofold and the presence of arteriolar narrowing (either generalised or focal) predicted a near threefold higher risk of CHD and support the use of direct ophthalmoscopy for cardiovascular risk stratification.
Management
In this case the patient went directly to accident and emergency (A&E) as he was extremely anxious about his loss of vision and due to the difficulty of obtaining an appointment with his GP. I discussed with him that this was not an ocular emergency and he should seek his GP's advice first, at the next available appointment. He insisted that he wanted to go directly to his local A&E and was given a letter with a photograph of the ocular findings and asked to return on conclusion of his visit at the hospital. The patient returned the following day and has since made an appointment to see his GP for a full blood work-up and to attend a follow-up appointment at the hospital in two weeks. Management of patients with a BRVO is also dependent upon intraocular pressures (IOPs). If the IOPs are within the normal range (10mmHg to 21mmHg), local protocol suggests that patients should be referred to their GMP for a full blood work-up at the next available appointment. If the IOPs are 30mmHg or more, patients should be referred as an ocular emergency to an A&E due to the increased risk of central vein occlusion.
Treatment
Treatment is dependent upon the cause of the visual loss. If visions do not spontaneously improve after retinal haemorrhaging has cleared and a clear view of the fundus is possible (usually three to six months after the event) a fluorescein angiogram is performed. If the visual loss is secondary to macular oedema due to leakage, argon laser photocoagulation in a grid pattern may be of benefit to the patient. If visual loss is due to macular ischemia (nonperfusion), then laser photocoagulation is usually not offered as treatment.6 Neovascularisation occurs in about 30 to 50 per cent of patients who have had significant areas of capillary nonperfusion following a BRVO.7 As neovascularisation is a serious complication, argon laser photocoagulation is usually indicated to prevent further vitreous haemorrhaging.
Medical treatment is not usually effective in treating BRVO. However, there have been cases where the use of intravitreal injections of triamcinolone has gained popularity among some vitreoretinal specialists due to its potent antipermeability and anti-inflammatory properties. Complications resulting from this treatment include cataract, raised IOPs, retinal detachment, infectious endophthalmitis and noninfectious endophthalmitis. Further studies are warranted to clarify the use of intravitreal triamcinolone as a management of macular oedema secondary to BRVO.8
Ocular symptoms can include:
? Sudden painless loss of vision
? Metamorphopsia
? Scotoma.
Ocular features include:
? Intraretinal haemorrhaging (usually flame shaped)
? Macular oedema
? Cotton-wool spots
? Respect of the horizontal raphe.
? Retinal neovascularisation.
? Vitreous haemorrhage with tractional retinal detachment. Traction may also cause retinal tears/breaks creating a combined rhegmatogenous and tractional retinal detachment.
? Neovascular glaucoma and neovascularisation at the disc (rare).9
Acknowledgements
Thank you to Deacon Harle and Carla Figueira for all their help and support.
References
1, 2, 6, 8, 9 Branch retinal vein occlusion www.emedicine.com/oph/topic386.htm [cited July 10 2006].
3 Bert-Jan H van den Born, Caroline AA Hulsman, Joost BL Hoekstra, Reinier O Schlingemann, Gert A van Montfrans. Value of routine fundoscopy in patients with hypertension: systemic review. www.Bmj.com June 11 2006
4 KJD Karki. Incidence of ophthalmoscopic fundus changes in hypertensive patients. Kathmandu University Medical Journal 2003, Vol 1, No. 1 27-31.
5 BB Duncan, TY Wong, HA Tyroler, CE Davis and FD Fuchs. Hypertensive retinopathy and the incident coronary heart disease in high risk men. Br J Ophthalmol, 2002;86;1002-1006 doi:10.1136/bjo.86.9.1002
7 Clinical Ophthalmoscopy. A Systemic Approach. Retinal Vascular Disorders. 3rd Edition. Butterworth Heinemann. Jack J. Kanski. Page 359.
Jonathan Bourton is staff optometrist/intern tutor at the Institute of Optometry