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Ординатура / Офтальмология / Английские материалы / Retinal Vein Occlusions_ Evidence-Based Management_Browning_2012.pdf
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13 Treatment of Retinal Vein Occlusions

With the same rationale as in CRVO, IH has also been used in the treatment of BRVO. The hematocrit is reduced to a target of 35% based on work demonstrating this hematocrit to be the optimum for oxygen delivery.45 In a randomized controlled clinical trial of 34 patients with BRVO, the IH group obtained statistically signiÞcantly better VA on average at the 1 year outcome than the control group (logMAR VA improvement of 0.43 vs. 0.17, P = 0.03).45 Of the IH group, 28% required GL for persistent macular edema compared to 44% for the control group (P > 0.05).45 In a case series of 30 patients, IH for 10 days achieved the intended goals of reduced hematocrit, plasma viscosity, and erythrocyte aggregation. The arteriovenous passage time of the affected sector of the retina on ßuorescein angiography on average fell 20%, whereas that of the unaffected sector did not change.232 On color Doppler imaging, the resistive index of the central retinal artery was decreased after hemodilution.285 As for CRVO and for the same reasons, IH has not been adopted for treatment of BRVO.161,231,253 The treatment has evolved, making it difÞcult to assess which parts have a beneÞcial effect Ð the hemodilution, the associated use of heparin, anti-vitamin K drugs, GL, or sector panretinal photocoagulation.231

13.1.4 Plasmapheresis

In certain cases of CRVO, serum immunoglobulin levels may be elevated, producing a hyperviscosity syndrome. Such cases may arise in the setting of connective tissue diseases such as systemic lupus erythematosus. In these instances, plasmapheresis has occasionally been used with anecdotal effectiveness.65

13.1.5Treatment

of Hyperhomocysteinemia in Patients with Retinal Vein Occlusions

Hyperhomocysteinemia and low plasma folate concentration have been associated with BRVO.295

A 1 ng/ml increase in plasma folate concentration is associated with an odds ratio for CRVO of 0.63 (protective effect), presumably through the intermediation of lowered plasma homocysteine.294 Plasma homocysteine is inßuenced by intake of folate and vitamins B6 and B12.40 In adults, supplementing folate intake by 0.5Ð5 mg/day reduces plasma homocysteine concentration approximately 25%. Supplementing vitamin B12 intake by 0.5 mg/day further reduces plasma homocysteine concentration approximately 7%.25,40 Therefore, the issue of reduction of plasma homocysteine by folate and B vitamin supplementation has been raised. There have been no randomized clinical trials that substantiate the efÞcacy of supplementing these vitamins on incidence of RVO, and the issue is controversial.40,284 Prospective studies would be worthwhile to guide clinical decision making.294,295

13.2Treatment of Previously Unsuspected Risk Factors for Retinal Vein Occlusion

Aside from attempting to reverse thrombosis in acute RVO, one aim of medical intervention is to determine if there are undetected systemic or ocular risk factors. If there are, such as hypertension or primary open-angle glaucoma, then ameliorating these risk factors may prevent subsequent RVO in the same or fellow eye (see Chap. 6).253

A common clinical scenario is for a patient with an RVO to have an elevated blood pressure in the ophthalmologistÕs ofÞce. It may be deduced that the patient has undetected hypertension. However, the deduction may be erroneous. The elevated blood pressure may be a response to emotional stress associated with the visual loss. If antihypertensive medication is prescribed and the patient is not hypertensive, the risk of iatrogenic arterial hypotension could aggravate the visual loss by exacerbating retinal hypoperfusion. This could be especially noteworthy in cases with concomitant cilioretinal arteriolar insufÞciency.102 It is probably wiser to refer the