Visual distortion or loss is the primary symptom of CRVO and can arise abruptly or gradually over a period of days or weeks. Pain is not usually present, unless complications such as glaucoma arise.

• Falling

  The central retinal thickness, however, was reduced in both groups, falling from 694 to 344 μm (1 month; p = 0.003,) to 361 μm (2 months; p = 0,002) and to 415 μm (3 months; p = 0,004) in the low visual acuity group and from 634 to 315 μm (1 month; p [ncbi.nlm.nih.gov]

  In the third millennium, the burdens of blindness and low vision, including associated comorbidities such as depression and risk of falls, are far more expensive than the costs and benefits of new drugs for retinal diseases. [healio.com]

  A fall in systemic arterial blood pressure would further lower the perfusion pressure. [ijo.in]

  Int Ophthalmol Clin. 2005 Fall. 45(4):153-61. [Medline]. Binder S, Aggermann T, Brunner S. Long-term effects of radial optic neurotomy for central retinal vein occlusion consecutive interventional case series. [emedicine.medscape.com]

• Severe Pain

  […] up anterior chamber angle structures, impedes flow of aqueous, and greatly elevates intraocular pressure ("neovascular glaucoma") Neovascular glaucoma causes severe pain, further loss of vision Pan-retinal photocoagulation, intraocular injection of anti-vascular [kellogg.umich.edu]

  It can cause severe pain and even more visual loss. Patients with CRVO are monitored closely for the growth of such blood vessels. [iowaretina.com]

• Macula

  Funduscopic examination of the right eye showed vascular tortuosity, scattered retinal hemorrhages, and retinal whitening in the macula. [ncbi.nlm.nih.gov]

  Left eye fundoscopy before intervention, showing swollen and elevated optic disc (D) with blurred disc margin, extensive flame-shaped haemorrhages (H), tortuous dilated vessels (V), and edematous macula (M). [oatext.com]

  […] into the macula. [bmcophthalmol.biomedcentral.com]

  The major cause of vision loss in CRVO is related to swelling and thickening of the macula, a part of the retina in the back of the eye. [noweyeknow.com]

• Retinal Hemorrhage

  CONCLUSION: The authors objectively evaluated retinal hemorrhagic patterns at the equator in eyes with acute central retinal vein occlusion using particle analysis. [ncbi.nlm.nih.gov]

• Rubeosis Iridis

  Ischemic CRVO’s can also lead to development of abnormal growth of blood vessels in the front of the eye on the iris (Rubeosis Iridis) and over the trabecular meshwork (drain for fluid to exit the eye). [retinacenternj.com]

  Neovascularization (abnormal new vessel formation) of the retina or iris (rubeosis iridis) occurs in about 16% of patients with central retinal vein occlusion and can result in secondary (neovascular) glaucoma, which can occur weeks to months after occlusion [msdmanuals.com]

  If vessel growth on the iris occurs (rubeosis iridis), these eyes may develop a very high pressure known as neovascular glaucoma due to obstruction of the fluid outflow channels. [williamsoneyeinstitute.com]

  Kaye SB, Harding SP (1988) Early electroretinography in unilateral central retinal vein occlusion as a predictor of rubeosis iridis. Arch Ophthalmol 106:353–356 PubMed Google Scholar 21. [link.springer.com]

  This may lead to profound vascular leakage, rubeosis iridis and raised intraocular pressure. The prognosis is extremely poor due to macular ischemia. [eyewiki.aao.org]

• Eye Pain

  A deeper or more intense eye pain needs to be reported to you physician immediately. [retinacenternj.com]

  Those with CRVO need to see an eye doctor at regular intervals to monitor for neovascular glaucoma and should be seen earlier and more frequently if there is a noticeable decrease in vision or eye pain. [preventblindness.org]

  […] is to keep the eye pain free. [mrcophth.com]

  Symptoms of Retinal Vein Occlusion include: Blurriness or loss of vision Floaters Eye pain It is very important to be evaluated by an ophthalmologist right away if you have any symptoms. [floridaretinainstitute.com]

  Pain in the eye: In severe cases of CRVO a blocked vein causes abnormal blood vessel growth on the iris and drainage channels in the front of the eye leading to painful pressure in the eye (neovascular glaucoma). [randeye.com]

• Visual Impairment

  Visual impairment as the initial symptom of leukemia, especially chronic myeloid leukemia, is rare, occurring in approximately 3% of all leukemias in children. [ncbi.nlm.nih.gov]

  A blockage in the retina that can lead to significant visual impairment RVO occurs when there is a blockage in the blood vessels of the retina, the light-sensitive nerve tissue lining the back of the eye. [pharma.bayer.com]

  All rig:10.1016/j.optm.2006.12.017eral central retinal., M.P.H.oint, New York.clusion (CRVO) is a common cause of visual impairment andof patients with CRVO are older than 50 years, and only 10%inal hypoxia in ischemic CRVO can stimulate neovascular-tion [docslide.net]

  This can lead to retinal detachment The new vessels also increase the intra-ocular pressure by clogging outflow of normal eye fluids, called neovascular glaucoma All these changes lead to visual impairment and blindness Non- ischemic CRVO: It is the most [dovemed.com]

• Scotoma

  BCVA rised to a level of 20/20 for the RE and the scotomas were disappeared immediately after using of the HBO treatment. [ncbi.nlm.nih.gov]

  The major sequel is a permanent central scotoma following on from cystoid macular edema. Neovascularization is unknown in this variant of the disease. Over 80% of patients with CRVO have this type. [news-medical.net]

  This applies particularly to an eye which has a visual field defect or a scotoma passing through or just involving the central fixation spot. (Eyes with nonischemic CRVO invariably have poor visual acuity due to central scotoma.) [webeye.ophth.uiowa.edu]

  Non-ischaemic CRVO is characterized by some loss of vision, metamorphopsia, slight impairment of the pupil responses to light and partial or complete central scotoma due to macular oedema. [medical-dictionary.thefreedictionary.com]

CRVO is not diagnosed directly with blood tests. These tests are carried out in order to detect a possible underlying condition, which could have led to the development of a central retinal vein occlusion in older individuals. In the younger population, blood tests are individualized and may include:

• Complete Blood Count
• Thrombophilia Screening - Proteins C and S, lupus anticoagulant, activated protein C, antithrombin III etc.
• Lipid profile
• Glucose tolerance
• protein electrophoresis

Imaging techniques are also a very helpful tool towards the detection of CRVO. A fundoscopic examination will illustrate retinal hemorrhaging of various degrees, profound edema and distended veins. A Color Doppler test has been also performed in the context of research [10], as it is able to reveal low blood flow, a piece of information that constitutes an indication for a future neovascularization process.

Optical coherence tomography scanning (OCT) is also a non-invasive procedure which can provide retinal measurements with great accuracy and identify macular edema [11] [12]. It is an important diagnostic tool because a profound hemorrhage prevents an angiography from detecting macular edema and without OCT, a crucial complication would be left undiagnosed.

• Hyperviscosity

  It can cause a hyperviscosity syndrome secondary to the paraproteinaemia associated with the disease. The increased hyperviscosity can lead to retinal vein occlusions and other ocular problems that may challenge clinicians. [ncbi.nlm.nih.gov]

• Hypercholesterolemia

  The central retinal vein occlusion was of nonischemic type and was associated with polyglobulia, hyperleukocytosis, hypercholesterolemia, multiple dental foci, and pulmonary sequelae of tuberculosis. [ncbi.nlm.nih.gov]

  Previous instances of patients with chronic central retinal vein occlusion (CRVO) and cystoid macular edema (CME) have been observed to spontaneously improve when placed on systemic niacin for hypercholesterolemia. [sutterhealth.org]

Intraocular injections of anti-VEGF medications or a dexamethasone implant are used to treat patients with CRVO and fovea-affecting macular edema. Anti-VEGF drugs hinder the production of the vascular endothelial growth factor that causes neovascularization and include ranibizumab, bevacizumab etc. Another sub-category of patients who benefit from the same treatment are those with CRVO and an acuity of >20/400 prior to the development of the occlusion. The latter group can also be treated with an intraocular injection of triamcinolone and an improvement of vision is to be expected in up to half of the patients.

Another possible treatment plan involves focal laser photocoagulation which is used to treat individuals with an occlusion of the branches of the retinal vein, even though this procedure is not effective to treat macular edema. The complication of neovascularization is treated with panretinal laser photocoagulation, in order to decrease vitreous hemorrhage and prevent neovascular glaucoma.

Prognosis is variable: it depends on the severity of the symptoms, the CRVO type and the clinical presentation at the time of diagnosis. Generally, non-ischemic CRVO that does not relapse into the ischemic type can regress spontaneously and vision is restored either to normal or almost normal in more than half of the patients, given that macular edema does not develop.

The majority of the patients will experience some visual loss. the best prognostic factor is good visual acuity (up to 20/40) at the time of diagnosis. Such a ratio is not likely to exhibit degradation. Acuity of 20/200 or worse, however, tends to stay poor, even after proper treatment and blood flow restoration.

As a general rule, a visual acuity that amounts to 20/60 or higher is expected to stay as it is, a 20/100-20/200 does have a margin of improvement but may fail to do so and an acuity <20/200 is not likely to increase.

Prognosis is unfavorable for patients with ischemic CRVO. Macular edema is a poor prognostic factor alongside neovascular glaucoma. A natural mechanism that can protect the individual from the development of neovascularization and glaucoma is the formation of opticociliary shunts.

CRVO is more common amongst people of older age (>50 years old) and rather uncommon amongst adolescents or young adults. Hypertension, diabetes, glaucoma and high blood viscosity can all provide the substrate for clot formation and CRVO. In some other cases, CRVO is an idiopathic condition.

Both the occlusion of the central retinal vein (CRVO) and of its branches are extremely common amongst the vascular disorders that affect the eye. CRVO's incidence has been estimated in a USA study to amount to 0,5% [6], whereas in Israel it appears to be 0.2% for people younger than 40 years old and 0.5% for people older than 64 years old. Australian epidemiologic studies have calculated the incidence of CRVO as amounting to a significant 4.6% in the age group of people that have surpassed the 80th year of their lives [7].

CRVO is more frequently observed in men, although the difference between men and women is not particularly significant. Mortality rates are not a useful calculation, as the condition itself does not lead to death. As far as the morbidity is concerned, however, it greatly depends on the type of the disease:

• Non-ischemic CRVO may regress spontaneously, followed by complete vision restoration. More than half of the patients, however, will eventually display poor visual acuity (20/200) and the possibility of a relapse into ischemic CRVO is present, even after a year following the original event.
• Ischemic CRVO is expected to lead to a 20/200 vision in over 90% of the patients and to neovascularization to more than 60% of the patients.

A second CRVO incident within the 2-year period after the initial event has been observed in 7% of the patients and affects the previously unaffected eye.

There appears not be no general consent regarding the pathophysiological mechanisms that lead to CRVO, which is thus considered to be a multifactorial disorder [8] [9].

Regarding the anatomy of the region, both the retinal vein and artery are in close proximity as they cross the restricted opening of the lamina cribrosa. the confined space may cause problems with blood flow and in the vascular walls, which will eventually lead to a thrombus formation. Additionally, an incidence of arterial sclerosis will exert extra pressure on the walls of the retinal vein as well, as the two are closely connected. Blood flow may be distorted, followed by significant alterations in the endothelium; both factors may also lead to the formation of a clot.

Another suggested mechanism include other types of external pressure exerted on the retinal vein walls, eg. due to density changed in the lamina cribrosa itself, or an optic nerve inflammation, given that the optic nerve is also at close proximity with the arterial and venous vessels. Coagulation disorders can naturally also play a part in the formation of thrombi, as can a hyperdynamic circulation pattern.

A significant complication of CRVO is neovascularization, which can lead to glaucoma and blindness in the affected eye. It has been attributed to the occlusion, which causes a retrograde venous flow to the retinal system and hypoperfusion. Hypoperfusion is believed to lead to the increased production of vascular endothelial growth factor (VEGF) in the vitreous cavity, which, in turn, causes neovascular activity both posteriorly and anteriorly. Another important complication involves macular edema, which is also thought to be a result of fluid loss from the vessels, caused by VEGF.

CRVO is caused by various underlying conditions. An appropriate treatment plan for these conditions and a responsible patient adherence to it can help prevent the development of CRVO. Regular visit to an ophthalmologist by patients with risk factors, such as diabetes and glaucoma, can also prove very beneficial.

Central retinal vein occlusion (CRVO) is a vascular disease affecting the central retinal vein. The clinical presentation of individuals affected by CRVO tends to fluctuate, with symptoms exhibiting great variability and different degrees of severity.

A general categorization divides CRVO into two distinct types, based on the effect it has on retinal perfusion: the ischemic type and non-ischemic type. Distinguishing the type of CRVO may be a challenge to the physician initially, as the symptomatology accompanying the condition alters with time. Non-ischemic CRVO causes no significant vision distortion and upon clinical examination, minor hemorrhaging of the retina is observed, alongside some cotton-wool spots and an adequate blood flow to the region. Vision is not expected to be impaired once non-ischemic CRVO regresses on its own, but there is a possibility that it will relapse into the ischemic type.

Ischemic CRVO, on the other hand, is a result of a complete occlusion of the vein. It is the severer counterpart type and upon clinical examination, substantial hemorrhage and cotton-wool spots are detected, as well as diminished blood flow of the retina. Symptoms may be accompanied by pain in the eye and vision is severely distorted or lost.

Generally, CRVO poses a considerable threat to vision, and every type of classification that has been proposed takes into consideration the region where inadequate blood flow is observed and the subsequent neovascularization [1] [2] [3] [4] [5]. An obstruction of the smaller branches of the retinal vein can also occur.

Diagnosis of CRVO is achieved through fundoscopy, optical coherence tomography and blood tests; the latter are performed with an aim to detecting the underlying disease. Treatment consists of intraocular injections of medications and focal laser photocoagulation, if the occlusion affects a branch of the central retinal vein. Neovascularization is treated with panretinal laser photocoagulation.

CRVO stands for central retinal vein obstruction. Each eye has two major vessels, which are responsible for the blood flow: the central retinal artery and vein. CRVO is a blockage of the blood flow in the central retinal vein, which stops the blood from exiting the retina and reaching the heart in order to be re-oxygenized. Blood remains in the region of the macula- an anatomical structure which mediated central vision- and causes problems with vision.

CRVO is a very common disorder of the eye. It can be caused by many underlying conditions, most commonly diabetes, glaucoma, arterial hardening (atherosclerosis) and coagulation disorders. In some cases the exact cause is not known.

There are two types of CRVO: the ischemic and non-ischemic type. The non-ischemic type is a mild form of the disease which does not result in complete vision loss and may go away on its own. The ischemic type is expected to cause significant vision distortion or even loss and causes much more damage to the eye structures. The primary symptom in CRVO is vision distortion without pain. If pain is present, this means that the complication of CRVO known as neovascular glaucoma has developed.

CRVO is treated with eye injections of various medications or laser photocoagulation, if only a smaller artery is affected and not the central one. If glaucoma secondary to CRVO arises, a laser therapy (panretinal photocoagulation) is performed. The underlying disease, if there is any, should be appropriately managed in order to avoid a CRVO recurrence, as well as a better outcome.

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2. Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology. 1983 May; 90(5):458-74.
3. Hayreh SS. Retinal vein occlusion. Indian J Ophthalmol. 1994 Sep; 42(3):109-32. 
4. Hayreh SS, Zimmerman MB, Podhajsky P. Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics. Am J Ophthalmol. 1994 Apr 15; 117(4):429-41. 
5. Williamson TH. Central retinal vein occlusion: what's the story?Br J Ophthalmol. 1997 Aug; 81(8):698-704.
6. Klein R, Moss SE, Meuer SM, et al. The 15-year cumulative incidence of retinal vein occlusion: the Beaver Dam Eye Study. Arch Ophthalmol. 2008 Apr; 126(4):513-8. 
7. Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia. The Blue Mountains Eye Study. Arch Ophthalmol. 1996 Oct; 114(10):1243-7.
8. David R, Zangwill L, Badarna M, et al. Epidemiology of retinal vein occlusion and its association with glaucoma and increased intraocular pressure. Ophthalmologica. 1988; 197(2):69-74. 
9. Ota M, Tsujikawa A, Kita M, et al. Integrity of foveal photoreceptor layer in central retinal vein occlusion.Retina. 2008 Nov-Dec; 28(10):1502-8.
10. Baxter GM, Williamson TH. Color Doppler flow imaging in central retinal vein occlusion: a new diagnostic technique?. Radiology. 1993 Jun; 187(3):847-50. 
11. Moschos MM, Moschos M. Intraocular bevacizumab for macular edema due to CRVO. A multifocal-ERG and OCT study. Doc Ophthalmol. 2008 Mar; 116(2):147-52. 
12. Gupta B, Grewal J, Adewoyin T, et al. Diurnal variation of macular oedema in CRVO: prospective study. Graefes Arch Clin Exp Ophthalmol. 2009 May;247(5):593-6.