Retinal vein thrombosis: pathogenesis and management

Abstract

To cite this article: Rehak M, Wiedemann P. Retinal vein thrombosis: pathogenesis and management. J Thromb Haemost 2010; 8: 1886-94.Summary. Retinal vein occlusion (RVO) is the most common retinal vascular disease after diabetic retinopathy. Owing to its multifactorial nature, however, management of this condition remains a challenge. Of the two main types of RVO, branch retinal vein occlusion (BRVO) is more prevalent than central retinal vein occlusion (CRVO). Most patients develop the disease at an elderly age, and more than half of them have associated systemic disorders (e.g. hypertension, hyperlipidemia and/or diabetes mellitus). There is no evidence to suggest routine testing for heritable thrombophilias in patients with RVO. The main cause of the visual impairment is macular edema, while neovascularization of the retina and optic disc are the most serious complications leading to vitreous hemorrhage, retinal detachment and neovascular glaucoma. Macular grid laser photocoagulation is an effective treatment for macular edema in patients with BRVO and a visual acuity of 20/40 or less. Other treatment options for reducing the edema are intravitreal steroids, anti-VEGF drugs and vitrectomy. The recently introduced intravitreal application of steroids and anti-VEGF drugs may prove to be a better approach for improving visual acuity. Finally, scatter panretinal laserphotocoagulation can effectively treat neovascularization and its secondary complications.

The Expanding Role of Vascular Endothelial Growth Factor Inhibitors in Ophthalmology

“…61 The pathophysiologic mechanisms leading to intravascular obstruction-occurring at arteriovenous crossings in BRVO and the lamina cribosa in CRVO-can be explained by the Virchow triad: hypercoagulability, hemodynamic changes (stasis and turbulence), and endothelial injury. 62 Impaired venous outflow causes retinal ischemia and VEGF synthesis with subsequent macular edema and retinal or iris neovascularization.…”

Retinal vein occlusion: time for action has come

“…However, the estimated incidence of RVO ranges between 0.53 and 1.6/1000 persons/year, an incidence that is comparable to that of ''more usual'' venous thromboembolic events, such as deep vein thrombosis of the lower limbs and pulmonary embolism [1,2]. Furthermore, RVO is one of the major causes of unilateral visual loss, and it seems to be associated with a significantly increased long-term risk of cardiovascular morbidity and mortality [3,4]. Unfortunately, despite this clear epidemiological and clinical burden, there is a substantial lack of adequate clinical studies upon RVO patients, and the optimal management of this disease remains a major unmet clinical need.…”

“…The direct management of sight-threatening complications in patients with RVO primarily involves the ophthalmologist with the potential application of different strategies including surgical approaches, laser therapy, the administration of intravitreal steroids or hemodilution, and other promising treatments such as intravitreal anti-vascular endothelial growth factor drugs [3,4,[6][7][8][9]. This management should also involve the internist when it comes to the choice of an antithrombotic drug, for both the short and the long-term treatment of RVO.…”

Laser Photocoagulation in Retinal Vein Occlusion

“…Wald [25] suggested that prophylactic scatter photocoagulation in ischaemic CRVO might prevent the risk of anterior segment neovascularization when 75 disc diameters or more of ischaemia are documented. On the other hand according to Mohamed et al [8] review of 17 Randomised clinical Trial results prophylactic PRPC does not prevent angle and iris neovascularization so does not totally eliminate risk of neovascular glaucoma for patient ischemic CRVO, but PRPC resulted in regression of angle and iris neovascularization and reduced progression to neovascular glaucoma ( Mitsch et al [26] demonstrated that PRPC leads to a slowly developing but reversible morphometric changes which are detected by spectral domain optical coherence tomography. They reported that this biological change indicates pan-retinal laser therapy cause diffuse, intense but reversible retinal inflammation.…”

“…Even RVO was first recognized over a century ago, the exact pathogenesis is not completely nderstood and therefore exact treatment methods not found yet. The condition may be due to a combination of three systemic changes known as Virchow's triad: (1) hemodynamic changes such as venous stasis; (2) degenerative changes of the vessel wall; and (3) blood hypercoagulability [6,8,9] . According to clinical findings, fundus appearance, Fluorescein angiography and electrophisiological results Hayreh futher divided RVO into three types: (1) BRVO is divided further into major BRVO (a) and macular BRVO (b) according to localization; (2) CRVO is divided into ischemic and non-ischemic types due to presence or absence of …”