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.
Other reports in this section
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Ischemic Central Retinal Vein Occlusion
Non-ischemic Hemi-central Retinal Vein Occlusion
Non-ischemic Branch Retinal Vein Occlusion
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