Retinal vein occlusion

Branch retinal vein occlusion (BRVO)
Prominent findings:
The main findings are superficial hemorrhages, retinal edema and cotton-wool spots in the areas draining into the occluded vein; the occluded vein is usually dilated and tortuous, and over time the adjacent artery becomes narrower. The most commonly involved area is the superotemporal one (two thirds of cases), and cases of nasal involvement are usually asymptomatic. There may be cases of involvement of half of the retina (hemispheric/hemicentral).

Pathogenesis

These usually occur in the area where the retinal vein and artery cross (AV crossing), because in this area the artery and vein share a common adventitia layer, and in situations where there is thickening of the artery walls, a narrowing of the vein and secondary venous thrombosis form. Subsequently, an occlusion of the artery in the same area can also develop.

Risk factors

The main risk factors identified in the Eye Disease Case-Control Study:

1. High blood pressure
2. Cardiovascular disease
3. Higher BMI at age 20
4. Glaucoma

The average age of the patients is about 60, and if the occlusion does not occur in the area of an AV crossing, then the possibility of retinochoroiditis should be taken into account.

Degree of vision impairment

The degree of vision impairment depends on the degree of ischemic damage in the macula. Fluorescein angiography can be used to identify the areas suffering from lack of perfusion. In some cases, the hemorrhages disappear over time and with the growth of new collaterals that can drain the edema. Extensive ischemic damage (over a diameter of 5 discs) leads to retinal or disc neovascularization in 40% of eyes, and of these, 2/3 will develop hemorrhages if photocoagulation is not performed. In summary — over 50% of patients will retain visual acuity above 20/40 a year after the event.

Findings that can be found in eyes with persistent vision impairment:

1. Ischemia of the macula
2. Cystoid macular edema
3. Hard lipid exudates
4. Subretinal fibrosis
5. Formation of an epiretinal membrane

A less common presentation is vision impairment on the background of vitreous hemorrhage or rhegmatogenous or tractional retinal detachment secondary to a retinal tear on the background of the neovascularization.

Treatment

Photocoagulation

Photocoagulation can be performed for three main indications:

1. Chronic macular edema — only in eyes with normal perifoveal perfusion, and usually one waits at least 3 months to give an opportunity for spontaneous absorption, and usually in eyes with vision between 20/40 and 20/200. Usually one focuses on the areas with edema that are drained by the occluded vessel.
2. Neovascularization of the posterior segment
3. Neovascularization of the iris — develops in 1% of cases — in such a case panretinal laser photocoagulation (PRP) can be performed in order to prevent glaucoma on the background of neovascularization (neovascular glaucoma).

Intraocular injections

Several studies have demonstrated the efficacy of intraocular injections of anti-VEGF agents in cases of BRVO (off-label use).

Central retinal vein occlusion (CRVO)

Prominent findings

The classic appearance is of dilated and tortuous blood vessels with a prominent optic disc that has blurred borders (swollen optic disc), accompanied by intraretinal hemorrhages and edema.

It is customary to divide it into two extremes:

a. Moderate degree (partial retinopathy or retinopathy with perfusion)

1. Without ischemic expression
2. Relatively preserved visual acuity
3. Mild RAPD

b. Severe degree (hemorrhagic retinopathy):

1. Extensive ischemia (10 times the size of the disc)
2. Poor visual acuity
3. Severe RAPD
4. Prominent central scotoma
5. Cotton-wool spots

80% of the in-between cases will eventually reach the severe degree.

60% of cases with a severe degree will develop iris neovascularization (3 months to half a year after the event).

90% of the patients are over the age of 50.

This may be accompanied by raised intraocular pressure, and there may also be shallowing of the anterior chamber to the point of an angle-closure glaucoma attack.

Pathogenesis

In most cases there is thrombosis of the central vein that extends beyond the lamina cribrosa, sometimes on the background of an atherosclerotic central retinal artery that presses on the vein and causes a thrombus. In rare cases, intraorbital pressure can lead to CRVO.

Risk factors:

a. High blood pressure

b. Diabetes

c. Open-angle glaucoma

A connection was found between contraceptive pills and diuretics and CRVO, and in addition it should be taken into account that states of hypercoagulability and hyperviscosity retinopathy can mimic a state of bilateral CRVO. In such a state, protein electrophoresis can be considered.

Follow-up tests

1. Measurement of intraocular pressure in order to detect glaucoma
2. Gonioscopy — to check for a tendency to angle closure, evidence of previous attacks, or neovascularization of the angle.

Treatment

1. Treatment of accompanying systemic diseases such as diabetes, hypertension, hyperlipidemia, hyperhomocysteinemia, and avoidance of smoking.
2. In patients without risk factors, and especially young patients, it is advisable to check for hereditary hypercoagulability risk factors in the family and to perform hypercoagulability tests.
3. These patients probably do not benefit from photocoagulation treatment.
4. Intraocular injections of anti-VEGF agents have proven to be an effective treatment in several studies conducted to date (off-label use).

Neovascularization of the iris (rubeosis)

The main risk factors:

a. Poor visual acuity

b. Extensive areas of ischemia

c. Extensive areas of intraretinal hemorrhage

Retinopathy of carotid occlusion

It can present with a picture that resembles CRVO, and the two can be distinguished by measurement with ophthalmodynamometry, which will demonstrate normal arterial pressure in CRVO and low pressure in partial occlusion of the carotids.