Retinal Vein Occlusion

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SIGNS AND SYMPTOMS

The patient will usually be elderly, often with a history of systemic

diseases such as diabetes and hypertension. The patient may be asymptomatic,

but often will complain of sudden painless unilateral loss of vision and/or

visual field, and 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, there may be a relative afferent pupillary defect.

Ophthalmoscopically, there will be retinal edema, superficial hemorrhages,

disc swelling, cotton wool spots, and tortuous and dilated retinal veins. If

there is a central retinal vein occlusion, these findings will encompass all

four retinal quadrants. A hemi-central retinal vein occlusion will involve

only the superior or inferior half of the retina. A branch retinal vein

occlusion will present with findings in only one quadrant, usually

supero-temporal, with the apex of the hemorrhage at an arteriovenous

crossing.

The hemorrhaging may be so severe that all features of the underlying retina

are obscured. Multiple cotton wool spots indicate retinal ischemia and

capillary non-perfusion. Anterior and posterior segment neovascularization

may occur later in the disease.

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 these factors.

The etiology of a branch retinal vein occlusion is an arteriolosclerotic

arteriole crossing and constricting the underlying venule. This will result

in leakage from the capillary beds draining into these vessels. The

capillary beds may be irreversibly damaged by this leakage, 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

substance. Vasoproliferative factors will then stimulate the proliferation

of neovascularization from nearby viable capillary beds.

In branch and hemi-central occlusions, neovascularization will most often

form on the optic disc or adjacent retina and 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 typically the posterior iris. This can lead

to rubeosis irides and neovascular glaucoma. In all cases of venous

occlusion, the main cause of vision decrease is macular edema. However, if

retinal capillary non-perfusion involves the perifoveal region, then vision

is dramatically and irreversibly lost.

MANAGEMENT

Fluorescein angiography, long held to be the gold standard in assessing

retinal vascular disease, has questionable use in vein occlusions. It is not

indicated initially, as the fresh hemorrhage will block transmission and

reveal no useful information, but later in the disease it will provide

information about retinal capillary perfusion and whether or not the

occlusion is ischemic and thus more likely to foster neovascularization. New

research indicates that ischemic retinal vein occlusions do not benefit from

prophylactic PRP; withhold this procedure until the patient develops frank

neovascularization of the iris, disc or retina.

Monitor the patient monthly with serial ophthalmoscopy, fundus photography

and goniscopy until you see resolution. If the patient has a hemi-central or

branch retinal vein occlusion and vision is below 20/40 due to macular

edema, the patient will benefit from focal laser photocoagulation anywhere

between three and 18 months after the occlusion's onset. Central retinal

vein occlusion patients with vision reduction due to macular edema do not

benefit from the proceudre, according to new research.

Due to the association of systemic disease with vein occlusions, co-manage

the patient with an internist. Tests to be ordered include: blood pressure,

fasting blood glucose, lipid and cholesterol studies, FTA-ABS, complete

blood count with differential, sickle dex (if the patient is

African-American), anti-nuclear antibodies, angiotensin converting enzymes,

and viscosity studies.

CLINICAL PEARLS

Ischemic vein occlusions are the only vein occlusions that will likely

develop neovascular complications, and they account for only one-third of

all occlusions.

Ischemic vein occlusions typically present with acuity worse than 20/200.

Those eyes with initial acuity better than 20/200 are at very low risk of

developing severe, permanent vision loss, and are likely to resolve.

Ischemic occlusions are likely to present with a relative afferent pupillary

defect. If not, then it is likely non-ischemic.

[Guest guest]

Thanks, Jill.

I'll send this to mom.

Barbara Uggen-

Editor, EDS Today

The Newsletter for, by, and about people with Ehlers Danlos Syndrome.

http://www.edstoday.org/

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