Retinal Vein Occlusion
Signs and Symptoms: The patient presenting with retinal vein occlusion will usually be elderly, often with systemic diseases such as diabetes and hypertension. He or she may be asymptomatic, but often will complain of a sudden painless unilateral loss of vision and/or visual field. The patient may complain of a sudden onset of floating spots or flashing lights. Acuity may range anywhere from 20/20 to finger counting. If vision loss is severe, a relative afferent pupillary defect may exist, indicative of retinal ischemia.
Ophthalmoscopically, you will note retinal edema, superficial hemorrhages, disc swelling, cotton-wool spots and tortuous and dilated retinal veins. With a central retinal vein occlusion (CRVO), these findings will appear in all four quadrants. A hemi-central retinal vein (HRVO) occlusion will involve only the superior or inferior half of the retina. A branch retinal vein occlusion (BRVO) will manifest these findings--although the tortuous veins may only appear in the most severe cases of BRVO--in only one quadrant; usually the superior-temporal sector, with the apex of the hemorrhaging at an arteriovenous crossing.
The hemorrhaging in any case may be so severe that all features of the underlying retina are obscured. The presence of multiple cotton wool spots indicates retinal ischemia and capillary non-perfusion. Anterior and posterior segment neovascularization may occur later in the course of the disease. Anterior segment neovascularization arises from cases of CRVO and posterior segment neovascularization more commonly occurs from BRVO or HRVO.
Pathophysiology: The etiology of central and hemi-central retinal vein occlusion is an obstruction of the central retinal vein, or one of the vein's two trunks, as it constricts through the lamina cribrosa. The cause is obscure, but may involve abnormal blood flow or blood constituents, atherosclerosis, vessel anomalies or a combination of factors.
The etiology of BRVO is an arteriolosclerotic arteriole crossing and constricting the underlying venule. This will result in leakage from the capillary beds draining into these vessels. This leakage may irreversibly damage the capillary beds, resulting in perpetual non-perfusion of the retinal tissue. If a significant area of capillary non-perfusion is present, then the occlusion is considered ischemic.
Loss of retinal capillary beds with subsequent retinal non-perfusion will lead to retinal hypoxia and the subsequent release of vasoproliferative chemicals. Vasoproliferative factors will then stimulate the proliferation of neovascularization from nearby viable capillary beds.
In the case of branch and hemi-central occlusions, neovascularization will most often form on the optic disc or adjacent retina. In such cases, neovascularization can lead to vitreous hemorrhage and tractional retinal detachment. In central retinal vein occlusions, the closest viable capillary network from which neovascularization will form is the posterior iris. This can lead to rubeosis irides and neovascular glaucoma.
In venous occlusion, macular edema is the main cause of vision loss. With macular edema, visual acuity is typically better than 20/200. However, if retinal capillary non-perfusion involves the perifoveal region, then vision is dramatically reduced (typically finger-counting) and irreversibly lost.
Management: Fluorescein angiography, while long held to be the gold standard in assessing retinal vascular disease, has questionable use in vein occlusions. This procedure is not indicated initially because the fresh hemorrhage will block transmission and reveal no useful information. Later in the course of the occlusion, angiography will give information about retinal capillary perfusion and whether or not the occlusion is ischemic and thus more likely to develop neovascular complications.
Research has indicated that ischemic retinal vein occlusions do not benefit from prophylactic pan-retinal photocoagulation. Withhold this procedure until the patient develops frank neovascularization of the iris, disc or retina.
If the patient has a hemi-central or branch retinal vein occlusion and vision is reduced below 20/40 due to macular edema, then the patient may benefit from focal laser photocoagulation anywhere between 3-18 months after the occlusion onset. CRVO patients with vision reduction due to macular edema do not benefit from focal laser photocoagulation.
Because vein occlusions are often associated with systemic disease, co-manage the patient with an internist. (For a list of tests to consider, see table.)
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