Branch retinal vein occlusionBMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e8373 (Published 10 December 2012) Cite this as: BMJ 2012;345:e8373
- Victor Chong, head of department
Retinal vein occlusion is one of the most common causes of sudden painless unilateral loss of vision. It is the second most common retinal vascular disease after diabetic retinopathy.1 Occlusion may occur in the central retinal vein or branch retinal vein.
Although specific ocular risk factors for central retinal vein occlusion include increased intraocular pressure and anatomical variation of the optic disc, systemic risk factors occur in patients with both types of occlusion.2 3 In a linked case-control study based on data from Danish national registries (doi:10.1136/bmj.e7885), Bertelsen and colleagues investigated comorbidity in patients with branch retinal vein occlusion.4 They were wise to study only patients with branch retinal vein occlusion because patients with central retinal vein occlusion may have ocular risk factors, so combining patients with both types of occlusion in one study of systemic risk factors could bias the findings.
Patients with retinal vein occlusion usually present with sudden loss of vision in one eye, which tends to get worse over the first few days. Some patients notice the loss of vision by chance when they cover one eye, but many have blurred vision when they wake up in the morning. The diagnosis is relatively straightforward. Funduscopy shows typical widespread retinal haemorrhages, in the whole fundus in central retinal vein occlusion or just a section of the retina in patients with branch retinal vein occlusion.
Loss of vision is usually secondary to macular oedema. Two treatments are licensed in Europe: dexamethasone implants and ranibizumab, with dexamethasone implants being approved by the National Institute for Health and Clinical Excellence in the United Kingdom. Aflibercept was recently approved by the Food and Drug Administration for treatment of central retinal vein occlusion in the United States. All are intravitreal injections that are generally well tolerated by patients.1
The mechanism of occlusion of the retinal vein is generally thought to be secondary to compression—particularly in branch retinal vein occlusion—by a thickened atherosclerotic retinal artery. The retinal arteries and veins run in close proximity to each other and cross over one another at several points in the retina. It is at these arteriovenous junctions that an artery with a thickened wall can displace the retinal vein or even compress the vein—arteriovenous nipping (or nicking)—a sign commonly seen in patients with hypertension. Compression of a retinal vein may disturb venous blood flow, leading to turbulence and endothelial damage by shear stress, and eventually to occlusion.
Bertelsen and colleagues chose cases of branch retinal vein occlusion from Danish secondary referral centres and confirmed each one by reviewing photographs of the fundus, which they rightly consider a reliable way to confirm the diagnosis.4 Using the national registry data they compared the 1168 cases with 116 800 randomly selected controls without the disease. One of the main criticisms of this paper is that the cases and controls were not matched for age—the controls were markedly younger, so the authors performed a statistical correction. Nonetheless, the study confirmed previous findings that hypertension and diabetes are more common in patients with branch retinal vein occlusion. The authors also found that peripheral artery disease, but not congestive heart failure or cerebrovascular disease, was more common in these patients. This is consistent with the hypothesis that systemic arterial diseases play an important role in the pathogenesis of this condition.
A somewhat surprising finding was that, after diagnosis, patients who did not already have these systemic risk factors were at higher risk of developing hypertension, diabetes, peripheral artery disease, congestive heart failure, and cerebrovascular disease. Patients with branch retinal vein occlusion were probably diagnosed as having these comorbidities at the same time or shortly after the diagnosis of branch retinal vein occlusion, which would also sit well with the current theory of pathogenesis.
Diagnosis of a comorbid disease, such as hypertension, is commonly made at the time of diagnosis of retinal vein occlusion. Primary care doctors are advised to investigate systemic risk factors when the diagnosis of branch retinal vein occlusion is made.1 Future studies should investigate the timing of the development of arteriopathic comorbidities discovered after the diagnosis of branch retinal vein occlusion. If comorbidities are diagnosed at that point or soon after, current management strategies, which include treatment of risk factors for arterial disease that are currently present, are acceptable. However, if comorbidities develop some years after the diagnosis of branch retinal vein occlusion in patients without systemic risk factors at the time of that diagnosis, it might be necessary to screen patients for risk factors of arterial disease for a longer period of time after diagnosis.
Cite this as: BMJ 2012;345:e8373
Competing interests: The author has completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.
Provenance and peer review: Commissioned; not externally peer reviewed.