AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Central retinal vein occlusion (CRVO) is a common retinal vascular disorder. Clinically, CRVO presents with variable visual loss; the fundus may show retinal hemorrhages, dilated tortuous retinal veins, cotton-wool spots, macular edema, and optic disc edema. In view of the devastating complications associated with the severe form of CRVO, a number of classifications were described in the literature. All these classifications take into account the area of retinal capillary nonperfusion and development of neovascular complications.

Broadly, CRVO can be divided into 2 clinical types, ischemic and nonischemic. In addition, a number of patients may have an intermediate in presentation with variable clinical course. On initial presentation, it may be difficult to classify a given patient into either category, since CRVO may change with time.

A number of clinical and ancillary investigative factors are taken into account for classifying CRVO, including vision at presentation, presence or absence of relative afferent pupillary defect, extent of retinal hemorrhages, cotton-wool spots, extent of retinal perfusion by fluorescein angiography, and electroretinographic changes.

Nonischemic CRVO is the milder form of the disease. It may present with good vision, few retinal hemorrhages and cotton-wool spots, no relative afferent pupillary defect, and good perfusion to the retina. Nonischemic CRVO may resolve fully with good visual outcome or may progress to the ischemic type.

Ischemic CRVO is the severe form of the disease. CRVO may present initially as the ischemic type, or it may progress from nonischemic. Usually, ischemic CRVO presents with severe visual loss, extensive retinal hemorrhages and cotton-wool spots, presence of relative afferent pupillary defect, poor perfusion to retina, and presence of severe electroretinographic changes. In addition, patients may end up with neovascular glaucoma and a painful blind eye.

Pathophysiology

The exact pathogenesis of the thrombotic occlusion of the central retinal vein is not known. Various local and systemic factors play a role in the pathological closure of the central retinal vein.

Central retinal artery and vein share a common adventitial sheath, as they exit the optic nerve head and pass through narrow opening in the lamina cribrosa. Because of this narrow entry in the lamina cribrosa, vessels are in a tight compartment with limited space for displacement. This anatomical position predisposes formation of thrombus in the central retinal vein by various factors, including slowing of blood stream, changes in the vessel wall, and changes in the blood.

Arteriosclerotic changes in the central retinal artery transforms the artery into a rigid structure and impinges upon the pliable central retinal vein, causing hemodynamic disturbances, endothelial damage, and thrombus formation. This mechanism explains the fact that there will be an associated arterial disease with CRVO. However, this association has not been proven consistently, and various authors disagree on this fact.

Thrombotic occlusion of the central retinal vein can occur as a result of various pathologic insults, including compression of the vein (mechanical pressure due to structural changes in lamina cribrosa, eg, glaucomatous cupping, inflammatory swelling in optic nerve, orbital disorders); hemodynamic disturbances (associated with hyperdynamic or sluggish circulation); vessel wall changes (eg, vasculitis); and changes in blood (eg, deficiency of thrombolytic factors, increase in clotting factors).

Occlusion of the central retinal vein leads to the backup of blood in the retinal venous system and increased resistance to venous blood flow. This increased resistance causes stagnation of blood and ischemic damage to the retina. It has been postulated that ischemic damage to the retina stimulates increased production of vascular endothelial growth factor (VEGF) in the vitreous cavity. Increased levels of VEGF stimulate neovascularization of the posterior and anterior segment (responsible for secondary complications due to CRVO). Also, it has been shown that VEGF causes capillary leakage leading to macular edema (which is the leading cause of visual loss in both ischemic CRVO and nonischemic CRVO).

Prognosis of CRVO depends upon reestablishment of patency of the venous system by recanalization, dissolution of clot, or formation of optociliary shunt vessels.

Frequency

United States

CRVO and branch retinal vein occlusion constitute the second most common retinal vascular disorder. The nonischemic type is more common than the ischemic type.

International

A large population-based study in Israel reported a 4-year incidence of retinal vein occlusion of 2.14 cases per 1000 of general population older than 40 years and 5.36 cases per 1000 of general population older than 64 years.

In Australia, prevalence of vein occlusion ranges from 0.7% in patients aged 49-60 years to 4.6% in patients older than 80 years.

Mortality/Morbidity

CRVO is not associated directly with increased mortality.

• Nonischemic CRVO may resolve completely without any complications in about 10% of cases. In about 50% of patients, vision may be 20/200 or worse. One third of patients may progress to the ischemic type, commonly in the first 6-12 months after presentation.
• In more than 90% of patients with ischemic CRVO, final visual acuity may be 20/200 or worse. Anterior segment neovascularization with associated neovascular glaucoma develops in more than 60% of cases. This can happen within a few weeks and up to 1-2 years afterward.
• It has been reported that the fellow eye may develop retinal vein occlusion in about 7% of cases within 2 years. In another report, the 4-year risk of developing second venous occlusion is 2.5% in the same eye and 11.9% in the fellow eye. Neovascular glaucoma may result in a painful blind eye.

Race

CRVO does not have any particular racial preference.

Sex

CRVO occurs slightly more frequently in males than in females.

Age

More than 90% of CRVO occurs in patients older than 50 years, but it has been reported in all age groups.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Direct review of systems toward various systemic and local factors predisposing the CRVO.

• Significant history includes the following:
• • Hypertension
  • Diabetes mellitus
  • Cardiovascular disorders
  • Bleeding or clotting disorders
  • Vasculitis
  • Autoimmune disorders
  • Use of oral contraceptives
  • Closed-head trauma
  • Alcohol consumption
  • Amount of physical activity
  • Primary open-angle glaucoma or angle-closure glaucoma
• Ocular symptoms at initial presentation
• • Asymptomatic
  • Decreased vision
  • Visual loss can be sudden or gradual, over a period of days to weeks. Visual loss ranges from mild to severe. Patients can present with transient obscurations of vision initially, later progressing to constant visual loss.
  • Photophobia
  • Painful blind eye
  • Redness of eyes
• Ocular symptoms in later stages
• • Decrease of vision
  • Pain in the eyes
  • Discomfort
  • Redness
  • Watering

Physical

Patients should undergo a complete eye examination, including visual acuity, pupillary reactions, slit lamp examination of the anterior and posterior segments, undilated examination of the iris, gonioscopy, fundus examination with indirect ophthalmoscope, and fundus contact lens.

• Visual acuity: Best-corrected vision always should be obtained. It is one of the important indicators of final visual prognosis.
• Pupillary reactions may be normal and may present with relative afferent pupillary reflex. If iris has abnormal blood vessels, pupil may not react.
• Conjunctiva: Advanced stages may show congestion on conjunctival and ciliary vessels.
• Cornea: Advanced stages may show diffuse corneal edema obscuring the visibility of internal structures.
• Iris may be normal. Advanced stages may show neovascularization. These vessels are detected best on an undilated iris. Initially, vessels may be seen around pupillary margins and peripheral iridectomy openings if present.
• Anterior chamber angle is examined by gonioscopy. This is examined best in an undilated iris. Initially, it may show neovascularization with open angles and later show total peripheral anterior synechia and closed angles.
• Fundus examination
• • Retinal hemorrhages may present in all 4 quadrants.
  • Hemorrhages can be superficial, dot and blot, and/or deep.
  • In some patients, hemorrhages may be seen in peripheral fundus only.
  • Hemorrhages can be mild to severe, covering the whole fundus giving a "blood and thunder appearance."
• Dilated tortuous veins: Veins may be dilated and tortuous.
• Optic disc edema: Optic disc may be swollen during early stage disease.
• Cotton-wool spots are more common with nonischemic CRVO. Usually, they are concentrated around the posterior pole. Cotton-wool spots may resolve in 2-4 months.
• Neovascularization of the disc
• • Fine abnormal neovascularization on the disc (NVD) or within 1 disc diameter from the disc may be present.
  • NVD indicates severe ischemia of the retina.
  • Sometimes NVD is difficult to differentiate from optociliary shunt vessels.
  • NVD can lead to preretinal or vitreous hemorrhage.
• Neovascularization elsewhere
• • Neovascularization elsewhere (NVE) is not as common as NVD.
  • NVE indicates severe ischemia of the retina.
  • NVE can lead to preretinal or vitreous hemorrhage.
• Optociliary shunt vessels are abnormal blood vessels on the disc, directing blood from retinal circulation to choroidal circulation, which indicate good compensatory circulation.
• Preretinal or vitreous hemorrhage
• Macular edema with or without exudates
• Cystoid macular edema
• Lamellar or full-thickness macular hole
• Optic atrophy
• Pigmentary changes in the macula

Causes

Central retinal vein obstruction has been associated with various systemic pathological conditions, although the exact cause and effect relationship has not been proven. Some of the conditions in which CRVO has been associated include the following:

• Systemic vascular disease
• • Hypertension
  • Diabetes mellitus
  • Cardiovascular disease
• Blood dyscrasias
• • Polycythemia vera
  • Lymphoma
  • Leukemia
• Clotting disorders
• • Activated protein C resistance
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Protein C
  • Protein S
  • Antithrombin III
• Paraproteinemia and dysproteinemias
• • Multiple myeloma
  • Cryoglobulinemia
• Vasculitis
• • Syphilis
  • Sarcoidosis
• Autoimmune disease - Systemic lupus erythematosus
• Oral contraceptive use in women
• Other rare associations
• • Closed-head trauma
  • Optic disc drusen
  • Arteriovenous malformations of retina
• The Eye Disease Case-Control Study Group reported that risk of CRVO is decreased in men with increasing level of physical activity and increasing levels of alcohol consumption. The same study group reported decreased risk of CRVO with use of postmenopausal estrogens and increased risk with higher erythrocyte sedimentation rates in women.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Hypertensive retinopathy
Retinopathy due to anemia
Retinopathy due to thrombocytosis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• No laboratory studies are indicated routinely in the diagnosis of CRVO.
• In older patients, laboratory testing should be directed toward identifying systemic vascular problems.
• In young patients, laboratory testing may be tailored depending upon individual findings, to include the following:
• • Complete blood count
  • Glucose tolerance test
  • Lipid profile
  • Serum protein electrophoresis
  • Chemistry profile
  • Hematologic tests
  • Syphilis serology
  • In addition, thrombophilia screening, activated protein C resistance, lupus anticoagulant, anticardiolipin antibodies, protein C, protein S, and antithrombin III may be completed.

Imaging Studies

• Color Doppler imaging is a noninvasive quantitative method of assessing the retrobulbar circulation. Detection of low venous velocities has been used to predict the onset of iris neovascularization. At present, this is performed as an investigational procedure in large facilities.
• Optical coherence tomography
• • Optical coherence tomography (OCT) scanning is a noninvasive, noncontact, transpupillary imaging technology that can image retinal structures in vivo with a resolution of 10-17 µm. OCT quantitatively measures the retina in micrometers in situ and in real time.
  • OCT can detect even subtle macular edema in the presence of significant hemorrhages, which is not evident by fluorescein angiography because of blockage from hemorrhage.
  • OCT is useful in quantitatively monitoring the development of macular edema and resolution with treatment.

Other Tests

• Fluorescein angiography is the most useful test for the evaluation of retinal capillary nonperfusion, posterior segment neovascularization, and macular edema.
• • Fluorescein angiography is one of the tests used in the classification of CRVO. Areas of capillary nonperfusion are visualized as hypofluorescence, but hemorrhages can block fluorescence and give a similar picture. Therefore, in early stages of the disease process, due to extensive hemorrhages, fluorescein angiography gives little information regarding the perfusion status of the retina. Once the hemorrhages clear, areas of capillary nonperfusion can be detected as hypofluorescence in the fluorescein angiography.
  • Various studies have reported different criteria for defining ischemic versus nonischemic CRVO based on extent of capillary nonperfusion of the retina. The amount of retinal nonperfusion ranges from 10-30 disc areas.
  • In addition, fluorescein angiography may show delayed arteriovenous transit, staining along the retinal veins, microaneurysms, arteriovenous collaterals, NVD, NVE, and dilated optic nerve head capillaries.
  • In a nonischemic central retinal vein obstruction, angiography may show minimal or absent retinal capillary nonperfusion, staining along the retinal veins, microaneurysms, and dilated optic nerve head capillaries. Resolved CRVO may be completely normal.
  • Macular edema may be detected as leakage from perifoveal capillaries, leakage from microaneurysms, or diffuse leakage on fluorescein angiography. If extensive edema is present, fluorescein angiography may show pooling of dye in large cystoid spaces. In addition, capillary nonperfusion around the fovea may indicate macular ischemia. If macular edema persists, pigmentary changes become evident.
• Electroretinography (ERG) is another useful test to evaluate functional status of the retina and to classify CRVO.
• • In ERG waveform, b wave and a wave are produced by the inner and outer retina, respectively.
  • In central retinal vein obstruction, perfusion of inner retina is affected, so that amplitude of the b wave is decreased relative to the a wave; the ratio of b to a has been shown to be reduced. Some studies indicate that a b-to-a ratio of less than 1 suggests an ischemic central retinal vein obstruction.

Histologic Findings

Not many histopathologic reports exist in the literature. A report of histologic sections of 29 eyes with central retinal vein obstruction showed a fresh or recanalized thrombus at or just posterior to the lamina cribrosa. Within the thrombi, a mild lymphocytic infiltration with prominent endothelial cells was seen. Loss of the inner retinal layers consistent with inner retinal ischemia also was seen.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

No known effective medical treatment is available for either prevention or the treatment of CRVO. Identifying and treating any systemic medical problems to reduce further complications is important. Because the exact pathogenesis of the CRVO is not known, various medical modalities of treatment have been advocated by multiple authors with varying success in preventing complications and preserving vision.

• The following is a list of those advocated treatments:
• • Aspirin
  • Anti-inflammatory agents
  • Isovolumic hemodilution
  • Plasmapheresis
  • Systemic anticoagulation with warfarin, heparin, and alteplase
  • Fibrinolytic agents
  • Systemic corticosteroids
  • Local anticoagulation with intravitreal injection of alteplase
• Intravitreal injection of triamcinolone
• • In patients with macular edema, injection of triamcinolone (0.1 mL/ 4 mg) into the vitreous cavity through pars plana has been shown to be effective not only in resolving the edema but also in corresponding improvement in vision.
  • Even though the exact mechanism of action of intravitreal injections of corticosteroids is not known, the triamcinolone crystals in the vitreous cavity probably reduce VEGF concentrations in the vitreous cavity. This leads to a reduction in capillary permeability and macular edema. The main drawback of an injection of triamcinolone was posttreatment recurrences of macular edema, requiring repeat triamcinolone injections, typically every 3-6 months.
  • In addition, significant complications reported due to the injection of triamcinolone include cataract, glaucoma, retinal detachment, vitreous hemorrhage, and endophthalmitis.
  • In view of most of the data available for the use of triamcinolone injection is because of multiple short-term follow-up studies, a large controlled, randomized clinical trial called the SCORE (Standard Care vs Corticosteroid for Retinal Vein Occlusion) Study is now underway in about 90 centers throughout the United States. This study is funded by the NEI to evaluate the use of intravitreal triamcinolone for macular edema in about 1,200 patients with CRVO or BRVO. All patients are being randomized to either 1 mg or 4 mg of triamcinolone versus standard care therapy (eg, observation in CRVO, laser photocoagulation in BRVO). Patients will be followed for up to 3 years to measure long-term treatment efficacy and safety; reinjections (if needed) will be performed beginning at 4 months after the initial therapy.

Surgical Care

Laser photocoagulation is the known treatment of choice in treatment of various complications associated with retinal vascular diseases (eg, diabetic retinopathy, branch retinal vein occlusion). Panretinal photocoagulation (PRP) has been used in the treatment of neovascular complications of CRVO for a long time. However, no definite guidelines exist regarding exact indication and timing of PRP. A National Eye Institute sponsored multicenter prospective study, the Central Vein Occlusion Study (CVOS), gave guidelines for treatment and follow-up care of patients with CRVO.

• Neovascularization: CVOS evaluated the efficacy of prophylactic PRP in eyes with 10 or more disc areas of retinal capillary nonperfusion, confirmed by fluorescein angiography, in preventing development of 2 clock hours of iris neovascularization or any angle neovascularization or whether it is more appropriate to apply PRP only when iris neovascularization or any angle neovascularization occurs. CVOS concluded that prophylactic PRP did not prevent the development of iris neovascularization and recommended to wait for the development of early iris neovascularization and then apply PRP.
• Argon green laser usually is used. Laser parameters should be about 500-µm size, 0.1-0.2 second duration, and power should be sufficient to give medium white burns. Laser spots are applied around the posterior pole, extending anterior to equator. They should be about 1 burn apart and total 1200-2500 spots.
• If ocular media is hazy for laser to be applied, cryoablation of the peripheral fundus is performed. About 16-32 transscleral cryo spots are applied from ora serrata posteriorly.
• Macular edema: CVOS evaluated the efficacy of macular grid photocoagulation in preserving or improving central visual acuity in eyes with macular edema due to central vein occlusion (CVO) and best-corrected visual acuity of 20/50 or poorer. Macular grid photocoagulation was effective in reducing angiographic evidence of macular edema, but it did not improve visual acuity in eyes with reduced vision due to macular edema from CVO. At present, the results of this study do not support a recommendation for macular grid photocoagulation for macular edema.
• Chorioretinal venous anastomosis
• • Chorioretinal venous anastomosis is performed by creating an anastomosis to bypass the site of venous occlusion in the optic disc. In this procedure, retinal veins are punctured, either using laser or by surgery, through the retinal pigment epithelium and the Bruch membrane into the choroid, thereby developing anastomotic channels into the choroid.
  • Chorioretinal venous anastomosis reduces macular edema and may improve vision in nonischemic CRVO. The success rate is low, and the complication rate can be quite high, including vitreous hemorrhages and choroidal neovascularization at the anastomosis site.
  • The exact indication and timing of the procedure has not been clearly studied.
• Radial optic neurotomy
• • Radial optic neurotomy is a new surgical technique in which a microvitreoretinal blade is used during pars plana vitrectomy to relax the scleral ring around the optic nerve. The central retinal artery and vein passes through the narrow openings of the cribriform plate in the optic disc.
  • Promoters of this technique suggest that CRVO may be due to the compression of the central retinal vein at this location creating a compartment syndrome. If this procedure is successful, it decompresses the closed compartment and leads to an improvement in venous outflow and a reduction of macular edema. No consistent results are available for this technique. Radial optic neurotomy can result in significant hemorrhage and neovascularization at the incision site in addition to regular complications of vitrectomy.
  • No consensus currently exists among various researchers regarding the exact criteria for the use of radial optic neurotomy.
• Vitrectomy
• • A vitrectomy is a technique in which the vitreous is surgically removed along with removal of the posterior hyaloid.
  • Some studies have shown that a vitrectomy may be beneficial for macular edema due to CRVO. One theory is that a vitrectomy may relieve traction on the macula and, thus, reduce macular edema. According to another hypothesis, removing the vitreous will also remove cytokines and VEGF associated with a venous occlusive event; thus, the stimulus for macular edema will be reduced.
  • At the present time, no convincing evidence indicates that a vitrectomy is the best approach.

Consultations

A general ophthalmologist should consult a retinal specialist for management of CRVO complications. They also should consult an internist for proper evaluation and management of any systemic medical problems. If patients develop neovascular glaucoma, a glaucoma specialist should be consulted.

Diet

Diet should be tailored to systemic medical problems.

Activity

No restrictions usually exist. If patients develop vitreous hemorrhage, they are advised to avoid strenuous activities, sleep with few pillows, and avoid bending and lifting heavy weights.

FOLLOW-UP

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Since neovascular complications and development of second venous occlusions can develop after CRVO, all these patients need follow-up care for long periods of time.
• CVOS recommended careful observation with frequent follow-up examinations in the early months for detection of iris neovascularization and prompt treatment.
• Patients with poor initial visual acuity should be monitored every month during the first few months and spaced thereafter, depending on course of the disease. These criteria apply more for patients with ischemic CRVO than with patients with nonischemic CRVO.
• With any associated complications, follow-up care should be individualized.

Deterrence/Prevention

• Optimal control of associated systemic diseases may reduce the incidence of similar occlusions in the fellow eye.
• Even though controversial, good control of intraocular pressure in patients known to have glaucoma may prevent CRVO.

Complications

• Ocular neovascularization
• • Anterior segment neovascularization leading to neovascular glaucoma
  • Posterior segment neovascularization leading to vitreous hemorrhage
• Macular edema
• • Macular edema is the common cause of decreased vision in CRVO, more so in the nonischemic type.
  • May resolve with good visual return
  • May develop permanent degenerative changes with poor visual prognosis
  • May develop cystoid macular edema leading to lamellar or full-thickness macular hole
• Cellophane maculopathy and macular pucker
• Optic atrophy

Prognosis

• Nonischemic CRVO
• • Complete recovery with good visual recovery occurs only in about 10% of cases.
  • Fifty percent of patients will have 20/200 or worse vision.
  • About one third of patients convert to ischemic CRVO. The CVOS group noted that of 547 eyes initially diagnosed to have nonischemic central retinal vein obstructions, 185 (34%) progressed to become ischemic central retinal vein obstructions within 3 years; 15% converted within the first 4 months.
• Ischemic CRVO
• • More than 90% of patients will have 20/200 or worse vision.
  • About 60% of patients develop ocular neovascularization with associated complications.
  • About 10% of patients can develop CRVO or other type of vein occlusions either within the same eye or contralateral eye within 2 years.

Patient Education

• Good control of systemic medical problems
• Regular medical and ophthalmologic checkups

MISCELLANEOUS

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• In view of multiple systemic problems these patients can have, it is important to refer patients to an appropriate specialist to avoid any legal ramifications.
• • Initially, these patients should be referred to an internist.
  • Patients may be referred to a retinal and glaucoma specialist as required to treat advanced problems.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Recent onset central retinal vein occlusion, showing extensive hemorrhages in the posterior pole giving the "blood and thunder appearance"
	View Full Size Image
Media type:  Photo

Media file 2:  Peripheral fundus view of the same patient in Picture 1, showing hemorrhages extending all over the fundus
	View Full Size Image
Media type:  Photo

Media file 3:  Fluorescein angiograph of the same patient in Picture 1, showing hypofluorescence due to blockage from hemorrhages in the retina. It is not useful to perform a fluorescein angiogram in acute stages of the disease.
	View Full Size Image
Media type:  Photo

Media file 4:  Fundus picture of the same patient in Picture 1, showing resolving neovascularization of the disc and panretinal photocoagulation scars
	View Full Size Image
Media type:  Photo

Media file 5:  Fluorescein angiogram of the same patient in Picture 1, taken more than 1 year later, showing persistent cystoid macular edema with good laser spots
	View Full Size Image
Media type:  Photo

Media file 6:  Patient with nonischemic central retinal vein occlusion presented with dilated, tortuous veins and superficial hemorrhages
	View Full Size Image
Media type:  Photo

Media file 7:  Fundus picture of the same patient in Picture 6, showing resolved hemorrhages and pigmentary changes in the macula several months later
	View Full Size Image
Media type:  Photo

Media file 8:  Central retinal vein occlusion showing significant disc edema with dilated tortuous veins and scattered retinal hemorrhages
	View Full Size Image
Media type:  Photo

Media file 9:  Fluorescein angiogram of the same patient in Picture 8, showing leakage from disc, staining of retinal veins
	View Full Size Image
Media type:  Photo

Media file 10:  Fundus of a patient with nonischemic central retinal vein occlusion, showing few scattered peripheral fundus hemorrhages
	View Full Size Image
Media type:  Photo

Media file 11:  Scattered retinal hemorrhages in a patient with central retinal vein occlusion
	View Full Size Image
Media type:  Photo

Media file 12:  Fluorescein angiogram of a patient with nonischemic central retinal vein occlusion, showing staining of dilated tortuous veins with leakage into macula in a cystoid pattern
	View Full Size Image
Media type:  Photo

Media file 13:  Fluorescein angiogram of the same patient in Picture 12, showing perifoveal capillary leakage in a cystoid pattern in late phases of angiogram
	View Full Size Image
Media type:  Photo

Media file 14:  Arteriovenous phase of fluorescein angiograph showing perifoveal capillary leakage in a patient with nonischemic central retinal vein occlusion
	View Full Size Image
Media type:  Photo

Media file 15:  Late phase of fluorescein angiograph of the same patient in Picture 13, showing cystoid pattern of leakage from perifoveal dilated leaking capillary network
	View Full Size Image
Media type:  Photo

Media file 16:  Fundus picture of a well-compensated, old central retinal vein occlusion showing optociliary shunt vessels
	View Full Size Image
Media type:  Photo

Media file 17:  Red-free photo of the same patient in Picture 16, showing prominent optociliary shunt vessels
	View Full Size Image
Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

• Bashshur ZF, Ma'luf RN, Allam S. Intravitreal triamcinolone for the management of macular edema due to nonischemic central retinal vein occlusion. Arch Ophthalmol. Aug 2004;122(8):1137-40. [Medline].
• Baxter GM, Williamson TH. Color Doppler flow imaging in central retinal vein occlusion: a new diagnostic technique?. Radiology. Jun 1993;187(3):847-50. [Medline].
• Beck AP, Ryan EA, Lou PL. Controversies regarding radial optic neurotomy for central retinal vein occlusion. Int Ophthalmol Clin. 2005;45(4):153-61. [Medline].
• Breton ME, Quinn GE, Keene SS, Dahmen JC, Brucker AJ. Electroretinogram parameters at presentation as predictors of rubeosis in central retinal vein occlusion patients. Ophthalmology. Sep 1989;96(9):1343-52. [Medline].
• Browning DJ, Rotberg MH. Vitreous Hemorrhage complicating laser-induced chorioretinal anastomosis for central retinal vein occlusion. Am J Ophthalmol. Oct 1996;122(4):588-9. [Medline].
• Catier A, Tadayoni R, Paques M. Characterization of macular edema from various etiologies by optical coherence tomography. Am J Ophthalmol. Aug 2005;140(2):200-6. [Medline].
• Cekic O, Chang S, Tseng JJ. Intravitreal triamcinolone treatment for macular edema associated with central retinal vein occlusion and hemiretinal vein occlusion. Retina. Oct-Nov 2005;25(7):846-50. [Medline].
• Central Vein Occlusion Study Group. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. The Central Vein Occlusion Study Group N report. Ophthalmology. Oct 1995;102(10):1434-44. [Medline].
• Central Vein Occlusion Study Group. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion. The Central Vein Occlusion Study Group M report. Ophthalmology. Oct 1995;102(10):1425-33. [Medline].
• Central Vein Occlusion Study Group. Central vein occlusion study of photocoagulation therapy. Baseline findings. Online J Curr Clin Trials. Oct 14 1993;Doc No 95:[Medline].
• Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. Aug 1993;111(8):1087-95. [Medline].
• Central Vein Occlusion Study Group. Natural history and clinical management of central retinal vein occlusion. [published erratum appears in Arch Ophthalmol 1997 Oct;115(10):1275]. Arch Ophthalmol. Apr 1997;115(4):486-91. [Medline].
• Central Vein Occlusion Study Group. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. The Central Vein Occlusion Study Group N report. Ophthalmology. Oct 1995;102(10):1434-44. [Medline].
• David R, Zangwill L, Badarna M, Yassur Y. Epidemiology of retinal vein occlusion and its association with glaucoma and increased intraocular pressure. Ophthalmologica. 1988;197(2):69-74. [Medline].
• Eccarius SG, Moran MJ, Slingsby JG. Choroidal neovascular membrane after laser-induced chorioretinal anastomosis. Am J Ophthalmol. Oct 1996;122(4):590-1. [Medline].
• Green WR, Chan CC, Hutchins GM. Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases. Retina. 1981;1:27-55.
• Hayreh SS, Zimmerman MB, Podhajsky P. Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics. Am J Ophthalmol. Apr 15 1994;117(4):429-41. [Medline].
• Hayreh SS. Retinal vein occlusion. Indian J Ophthalmol. Sep 1994;42(3):109-32. [Medline].
• Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology. May 1983;90(5):458-74. [Medline].
• Ip MS, Gottlieb JL, Kahana A. Intravitreal triamcinolone for the treatment of macular edema associated with central retinal vein occlusion. Arch Ophthalmol. Aug 2004;122(8):1131-6. [Medline].
• Leizaola-Fernandez C, Suarez-Tata L, Quiroz-Mercado H. Vitrectomy with complete posterior hyaloid removal for ischemic central retinal vein occlusion: series of cases. BMC Ophthalmol. May 20 2005;5(1):10. [Medline].
• Luttrull JK. Epiretinal membrane and traction retinal detachment complicating laser- induced chorioretinal venous anastomosis. Am J Ophthalmol. May 1997;123(5):698-9. [Medline].
• McAllister IL, Constable IJ. Laser-induced chorioretinal venous anastomosis for treatment of nonischemic central retinal vein occlusion. Arch Ophthalmol. Apr 1995;113(4):456-62. [Medline].
• Mirshahi A, Roohipoor R, Lashay A. Surgical induction of chorioretinal venous anastomosis in ischaemic central retinal vein occlusion: a non-randomised controlled clinical trial. Br J Ophthalmol. Jan 2005;89(1):64-9. [Medline].
• Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia. The Blue Mountains Eye Study. Arch Ophthalmol. Oct 1996;114(10):1243-7. [Medline].
• Opremcak EM, Bruce RA, Lomeo MD. Radial optic neurotomy for central retinal vein occlusion: a retrospective pilot study of 11 consecutive cases. Retina. 2001;21(5):408-15. [Medline].
• Weizer JS, Stinnett SS, Fekrat S. Radial optic neurotomy as treatment for central retinal vein occlusion. Am J Ophthalmol. Nov 2003;136(5):814-9. [Medline].
• Williamson TH. Central retinal vein occlusion: what''s the story?. Br J Ophthalmol. Aug 1997;81(8):698-704. [Medline].

Article Last Updated: Feb 16, 2006