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 Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 3  |  Page : 303-307

A classic case of ischemic central retinal vein occlusion with macular edema

Department of Ophthalmology, Rangaraya Medical College, Kakinada, Andhra Pradesh, India

Date of Submission16-Feb-2021
Date of Acceptance10-May-2021
Date of Web Publication03-Sep-2021

Correspondence Address:
Mr. Tarun Kumar Suvvari
Department of Ophthalmology, Rangaraya Medical College, Pithampuram Road, Kakinada 533001, Andhra Pradesh.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mgmj.mgmj_13_21

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Central retinal vein occlusion (CRVO) is a significant cause of marked or total loss of vision in the middle-aged and elderly population. The patient was a 54-year-old man with a history of uncontrolled diabetes and was given seven intravitreal bevacizumab (Avastin) injections as treatment. The patient was advised to follow-up during the next 6 months, including gonioscopy and undilated examination of the iris to look for the iris/disc neovascularization. We presented a classic case of unilateral ischemic CRVO with macular edema, in whom diabetes is the leading risk factor. Close follow-up and diabetes control are advisable to prevent a similar scenario.

Keywords: Bevacizumab, central retinal vein occlusion (CRVO), diabetes, fluorescein angiogram, macular edema, unilateral ischemic CRVO

How to cite this article:
Mantha MK, Suvvari TK, Kotipalli LN, Kota T. A classic case of ischemic central retinal vein occlusion with macular edema. MGM J Med Sci 2021;8:303-7

How to cite this URL:
Mantha MK, Suvvari TK, Kotipalli LN, Kota T. A classic case of ischemic central retinal vein occlusion with macular edema. MGM J Med Sci [serial online] 2021 [cited 2022 Jan 25];8:303-7. Available from: http://www.mgmjms.com/text.asp?2021/8/3/303/325531

  Introduction Top

Central retinal vein occlusion (CRVO) is a significant cause of marked severe vision impairment and blindness, mostly in adults. After diabetic retinopathy, CRVO is the second most common cause of blindness. The predominant associated factors are hypertension, diabetes mellitus, hyperlipidemia, hyperhomocysteinemia, glaucoma, etc.[1],[2]

Thrombosis of the central retinal vein leads to venous stasis, leading to disc swelling, diffuse nerve fiber layer, pre-retinal hemorrhage, and cotton wool spots that create a dramatic appearance called blood thunder fundus. The prevalence of CRVO is 0.7% in population-based studies. The population-based study formed a cumulative incidence of 0.5% over 15 years, with a prevalence of 1.3% for people aged 65 and older.[2],[3]

CRVO is seen most commonly with raised intraocular pressure and glaucoma. In contrast to central retinal arterial occlusion (CRAO), the onset of vision loss is typically subacute but severe. If venous stasis is severe, there are chances of infarction due to slow blood flow on the arterial side.

  Case report Top

A 54-year-old male patient presented to the hospital with decreased and blur vision in the left eye. We observed no redness, swelling, and pain in the eye. He had a history of diabetes mellitus (uncontrolled). He was initially on glimepiride, but now takes Glimfirst M1, a combination of glimepiride and metformin. His vital signs were stable and general examination was normal.

An ophthalmologic examination showed visual acuity of 20/20 in the right eye and 20/63 in the left eye. Pupil reaction showed a sluggish reactive pupil in the left eye. Intraocular pressures were16 mmHg in the right eye and 14 mmHg in the left eye. Fundus examination of the left eye showed a normal cup-to-disc ratio. It dilated tortuous retinal veins with intra-retinal hemorrhages, and the right eye showed otherwise normal optic disc and flat macula.[4]

A color fundus photograph of the left eye revealed superficial opacification of the retina[4] mainly in the macular area with a combination of multiple dot-blot and flame-shaped hemorrhages in all four quadrants [Figure 1]. Fluorescein angiogram of the left eye showed blocked venous fluorescence from retinal hemorrhage extensive areas of capillary non-perfusion vessel wall staining [Figure 2]. Here, macular thickness was measured by optical coherence tomography, and all the nine parameters were far more raised than the normal values, which is in macular edema [Figure 3].
Figure 1: Color fundus photograph of the left eye revealed superficial opacification of the retina

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Figure 2: Fluorescein angiogram of the left eye

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Figure 3: Macular thickness measured using optical coherence tomography

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Results of laboratory tests of the patient are represented in [Table 1]. The patient was prescribed bevacizumab (Avastin) intravitreal injections. A total of seven injections (each per month) of intravitreal bevacizumab of a dosage of 1.25 mg were given. Not a complete recovery of vision occurred. The visual acuity of the left eye was found to be 20/50. He was also suggested brimonidine, timolol, moxifloxacin, and fluorometholone for the betterment of eye vision and to prevent any bacterial infection further. The patient was followed up for the next 6 months, including gonioscopy and undilated examination of the iris to find any neovascularization of the iris/disc.[4]
Table 1: Laboratory values of the patient

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Differential diagnosis includes ocular ischemic syndrome, diabetic retinopathy, papilledema, radiation retinopathy, and retinopathy due to anemia.

  Discussion Top

CRVO is of two types:

  • Non-ischemic: 81% of CRVO initially belong to this category.

  • The site of occlusion site in the central retinal vein is neither in the lamina cribrosa nor in the adjacent retrolaminar region. Severity depends on the site of occlusion,[5] and is characterized by a vision that is better than 20/200, defined as <10 disc diameter (DD) of capillary non-perfusion.[6]

  • Ischemic: The occlusion site is in the region of lamina cribrosa (or) immediately posterior to that.[5] It is defined as >10 DD of non-perfusion patients who are usually older and have low vision; 60% develop iris neovascularization (INV), up to 33% develop neovascular glaucoma (NVG), 10% combine with retinal branch occlusion (usually cilioretinal artery due to low perfusion pressure of the choroidal system).[6]

  • In some patients, non-ischemic CRVO turns to ischemic overnight or gradually.[5] CRVO is a disease of the old population (age >50 years old). Major risk factors include hypertension, atherosclerosis, and diabetes. Other risk factors include glaucoma, syphilis, sarcoidosis, vasculitis, increased intra-orbital or intraocular pressure, hyphema, and hyperviscosity syndromes. Other factors may also affect the natural history of CRVO.[7]

    Demographic factors include age or gender, systemic factors include vascular risk factors/high levels of blood hematocrit, and ocular factors such as pigment changes in the macula, epiretinal-membrane formation in long-standing macular edema, retinal collaterals, and glaucoma have been reported to be associated with poor functional outcomes.[8] O’Mahoney et al.’s[9] study revealed the relationship between traditional atherosclerosis risk factors and RVO. They concluded that diabetes is one of the main risk factors for CRVO following hyperlipidemia and hypertension.

    Risk factors for initiation of NVG in an eye with CRVO are hypertension, worse visual acuity on presentation, and relative afferent pupillary defect (RAPD).[10] Lowering intraocular pressure helps to improve retinal circulation in an eye with CRVO. There is a risk of 10% for the development of BRVO or CRVO in the fellow eye.[11],[12]

    Visual acuity in patients diagnosed with CRVO at baseline is a strong early predictor for the development of INV/angle neovascularization (ANV), as it is the amount of non-perfusion seen by fluorescein angiogram.[13] Currently, regular monitoring is recommended in patients with ischemic CRVO for the development of INV or ANV, for which pan-retinal laser photocoagulation (PRP) is the mainstay treatment.[14]

    But the data of central vein occlusion study (CVOS) did not support the recommendation for prophylactic PRP. The CVOS revealed that early PRP decreased the rate of INV.[13] However, the reduction was not statistically significant. The CVOS recommended physicians for close follow-up of eyes with CRVO during the initial 6 months (including gonioscopy and undilated slit lamp examination of the iris) and prompt PRP of eyes in which INV/ANV develops.[4] Compared to selective PRP or photodynamic therapy (PDT), PRP is better at determining INV and anterior segment neovascularization regression; PDT can also be used safely in management.[15]

      Conclusion Top

    Our case illustrates an exciting presentation of ischemic CRVO with macular edema leading to an impaired vision where diabetes is thought to be the main risk factor. We focussed on controlling diabetes as preventive measure to protect the fellow eye. Meanwhile, close follow-up was stressed for investigating the signs of INV/ANV.

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    Conflicts of interest

    There are no conflicts of interest.

      References Top

    Natural history and clinical management of central retinal vein occlusion. The Central Vein Occlusion Study Group. Arch Ophthalmol1997;115:486-91. doi: 10.1001/archopht.1997.01100150488006.  Back to cited text no. 1
    RVO Guidelines—2015 by the Royal College of Ophthalmologists. Available from: https://www.rcophth.ac.uk/wp-content/uploads/2015/07/Retinal-Vein-Occlusion-RVO-Guidelines-July-2015.pdf. Accessed Jan 10, 2021.  Back to cited text no. 2
    Mohamed Q, McIntosh RL, Saw SM, Wong TY. Interventions for central retinal vein occlusion: An evidence-based systematic review. Ophthalmology 2007;114:507-19, 524.  Back to cited text no. 3
    Alasil T, Rauser ME. Intravitreal bevacizumab in the treatment of neovascular glaucoma secondary to central retinal vein occlusion: A case report. Cases J 2009;2:176.  Back to cited text no. 4
    Hayreh SS. Retinal vein occlusion. Indian J Ophthalmol 1994;42:109-32.  Back to cited text no. 5
    [PUBMED]  [Full text]  
    Freidman N, Kaiser P, Trattler W. Central Retinal Vein Occlusion. Review of Ophthalmology. 1st ed., Chapter 11. Edinburgh: Elsevier Inc.; 2005. p. 329.   Back to cited text no. 6
    Bhagat N, Goldberg MF, Gascon P, Bell W, Haberman J, Zarbin MA. Central retinal vein occlusion: Review of management. Eur J Ophthalmol 1999;9:165-80.  Back to cited text no. 7
    Jonas JB. Intravitreal triamcinolone acetonide: A change in a paradigm. Ophthalmic Res 2006;38:218-45.  Back to cited text no. 8
    O'Mahoney PRA, Wong DT, Ray JG . Retinal vein occlusion and traditional risk factors for atherosclerosis. Arch Ophthalmol2008;126:692-9. 10.1001/archopht.126.5.692.  Back to cited text no. 9
    Rong AJ, Swaminathan SS, Vanner EA, Parrish RK II. Predictors of neovascular glaucoma in central retinal vein occlusion. Am J Ophthalmol 2019;204:62-9.  Back to cited text no. 10
    Hayreh SS. Prevalent misconceptions about acute retinal vascular occlusive disorders. Prog Retin Eye Res 2005;24:493-519.  Back to cited text no. 11
    Baseline and early natural history report. The Central Vein Occlusion Study. Arch Ophthalmol1993;111:1087-95.  Back to cited text no. 12
    A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. The Central Vein Occlusion Study Group N Report. Ophthalmology 1995;102: 1434-44.  Back to cited text no. 13
    Siehyean K, Ting DSW, Fekrat S, Scott IU. Retina ophthalmic pearls: Diagnosis and management of central retinal vein occlusion. Eyenet Magazine 2018;1:33-5. Available from: www.aao.org › january-2018-ophthalmic-pearls-pdf.  Back to cited text no. 14
    Parodi MB, Friberg TR, Pedio M, Fiotti N, Di Stefano G, Ravalico G. Panretinal photocoagulation and photodynamic therapy for anterior segment neovascularization secondary to ischemic central retinal vein occlusion. Ophthalmic Surg Lasers Imaging 2007;38:94-9.  Back to cited text no. 15


      [Figure 1], [Figure 2], [Figure 3]

      [Table 1]


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