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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 2  |  Issue : 2  |  Page : 445-447

Unilateral proliferative diabetic retinopathy following central retinal vein occlusion


Shri Bhagwan Mahavir Vitreoretinal Services, Sankara Nethralaya, Chennai, Tamil Nadu, India

Date of Submission17-May-2021
Date of Acceptance24-Sep-2021
Date of Web Publication13-Apr-2022

Correspondence Address:
Muna Bhende
Shri Bhagwan Mahavir Vitreoretinal Services, Sankara Nethralaya, 18 College Road, Chennai, - 600 006, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_1223_21

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  Abstract 


This case report describes a diabetic patient with nonischemic central retinal vein occlusion who developed findings suggestive of proliferative diabetic retinopathy in the same eye, with a normal retina in the right eye 3 years after presentation.

Keywords: Central retinal vein occlusion, macular edema, proliferative diabetic retinopathy


How to cite this article:
Mohan S, Bhende M. Unilateral proliferative diabetic retinopathy following central retinal vein occlusion. Indian J Ophthalmol Case Rep 2022;2:445-7

How to cite this URL:
Mohan S, Bhende M. Unilateral proliferative diabetic retinopathy following central retinal vein occlusion. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jul 6];2:445-7. Available from: https://www.ijoreports.in/text.asp?2022/2/2/445/342871



Posterior segment neovascularization is rare in central retinal vein occlusion (CRVO) compared to anterior segment neovascularization. Ocular neovascularization is not known to develop in nonischemic CRVO (NI-CRVO) unless it converts to ischemic CRVO. We describe a diabetic patient with NI-CRVO who developed retinal neovascularization typical of proliferative diabetic retinopathy (PDR) in the same eye 3 years after presentation.


  Case Report Top


A 51-year-old gentleman presented with complaints of diminished vision in the left eye for 2 months in 2015. He was a known diabetic for 8 years duration on oral hypoglycemic medications. His best-corrected visual acuity (BCVA) was 20/20, N6 in OD and 20/120, N18 in OS. Intraocular pressure (IOP) and pupillary reactions in both eyes were normal. Gonioscopy findings were suggestive of primary angle closure and Yag peripheral iridectomy (PI) was done in both eyes, and the patient was started on topical antiglaucoma medications in both eyes post Yag PI. Right eye fundus was normal [Figure 1]a and [Figure 1]c. Left eye fundus revealed dot, blot, and flame-shaped hemorrhages in all quadrants, dilated and tortuous retinal veins, and macular edema suggestive of CRVO [Figure 1]b and [Figure 1]d. Systemic evaluation did not reveal any abnormalities other than preexisting diabetes. Over 8 months, he received two monthly doses of ranibizumab 0.5 mg in 0.05 mL followed by two monthly doses of bevacizumab 1.25 mg in 0.05 mL as there was no response to ranibizumab. As there was no response to bevacizumab, he was given intravitreal ozurde × 0.7 mg. On day 1, post ozurdex injection, the IOP was 14 mmHg. Subsequently, he developed persistent raised IOP ranging between 30 and 38 mmHg. Despite topical antiglaucoma medications, due to high IOP attributed to a combination of steroid response and preexisting primary angle closure he underwent trabeculectomy with mitomycin C in the left eye in November 2016. For persisting macular edema, he underwent two sittings of grid laser in 2017 following which the edema reduced and remained so till the last visit. There was a significant reduction in the macular edema post laser.
Figure 1: (a-d) At first presentation: (a) Fundus photo of the right eye which is within normal limits. (b) Fundus photo of the left eye showing dot, blot, and flame-shaped hemorrhages in all quadrants, dilated, and tortuous retinal veins and macular edema. (c) OCT of the right eye which shows normal foveal contour. (d) OCT of the left eye showing altered foveal contour with gross cystoid macular edema and subfoveal fluid

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In July 2018, his BCVA was 20/20, N6 in OD and 20/80, N12 in OS. Right eye fundus was normal with no evidence of diabetic retinopathy [Figure 2]a and [Figure 2]c. The left eye fundus had features of PDR with hard exudates at the macula, multiple hemorrhages, microaneurysms, and neovascularization elsewhere (NVE) [Figure 2]b and [Figure 2]d. There was no neovascularization of iris or angle in either eye. Fundus fluorescein angiography was performed and did not show any DR changes in the right eye [Figure 3]a. The left eye showed evidence of PDR [Figure 3]b and [Figure 3]c. In view of gross asymmetry of DR, a carotid and orbital doppler was performed, which was normal except for slow flow in the left ophthalmic artery. He underwent three sittings of pan retinal photocoagulation (PRP) for left eye PDR in July 2018 and fill in PRP for persistent neovascularization and preretinal hemorrhage in August 2020 [Figure 4]b. The IOP in OS was controlled without need for topical medications.
Figure 2: (a-d) At 3 years follow-up. (a) Fundus photo of the right eye which is within normal limits. (b) Fundus photo of the left eye showing hard exudates at the macula, multiple hemorrhages, microaneurysms, and neovascularization elsewhere (NVE). (c) OCT of the right eye which shows normal foveal contour. (d) OCT of the left eye showing a normal foveal contour, with no macular edema, intraretinal hyper reflective dots temporal to the fovea corresponding to the hard exudates

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Figure 3: (a-c) At 3 years follow-up. (a) FFA of the arteriovenous phase of right eye which is within normal limits. (b) FFA of the arteriovenous phase of the left eye showing the presence of microaneurysms, capillary nonperfusion, and neovascularization elsewhere. Macular grid laser scars are noted. (c) FFA of the late phase of the left eye showing leaking neovascularization elsewhere. No macular edema is seen

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Figure 4: (a-d) At 5 years follow-up. (a) Fundus photo of the right eye which is within normal limits. (b) Fundus photo of the left eye showing lasered PDR, resolving hard exudates and no macular edema, preretinal hemorrhage. (c) OCT of the right eye which shows normal foveal contour. (d) OCT of the left eye showing a normal foveal contour, with no macular edema and presence of a posterior vitreous detachment

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At last follow-up in December 2020, 5 years after the diagnosis of CRVO, his BCVA was 20/20, N6 in OD and 20/120, N18 in OS. IOP was normal in both eyes. Anterior segment did not show any neovascularization. The right fundus showed no evidence of DR [Figure 4]a and [Figure 4]c. The left eye fundus showed lasered PDR with regressing NVE, resolving hard exudates and no macular edema [Figure 4]d.


  Discussion Top


Ocular neovascularization can occur in patients with CRVO. Patients with ischemic CRVO (>10 disk areas of capillary nonperfusion in the retina) are at higher risk of neovascularization. When ocular neovascularization develops, the commonest site is the anterior segment in the form of neovascularization of iris or angle. Posterior segment neovascularization is extremely rare and usually involves the optic disc. Anterior segment neovascularization occurs within 6–7 months compared to disc neovascularization which takes 12 months from onset and retinal neovascularization which takes 24 months from onset. Therefore, in ischemic CRVO, the risk of development of anterior segment complication (i.e., NVG) is much higher and earlier than complication of posterior segment (e.g., vitreous hemorrhage).[1]

Hayreh and Zimmerman found that in patients with ischemic CRVO, the development of retinal neovascularization is 9% and over disc is 6% compared to 49% iris neovascularization and 37% angle neovascularization. More severe the ischemia, higher the chances of developing neovascularization.[1] NI-CRVO is not known to be associated with neovascularization unless there is ocular ischemia or coexistent DR. DR develops much earlier in eyes with NI-CRVO than in fellow eyes without NI-CRVO. Hayreh and Zimmerman suggested that neovascularization seen in these eyes later is because of DR and not because of nonischemic CRVO as seen in five eyes in their study.[1] In one study, Hayreh found that in diabetics, NI-CRVO retinopathy often gradually merges into the development of DR in the involved eye only, as if CRVO acts as an additive effect to stimulate development of DR earlier than would have occurred otherwise.[2]

Asymmetric DR is not common. It occurs in 5–10% of patients with DR and usually signifies significant carotid artery disease. Asymmetric DR has been described in association with previous branch retinal vein occlusion, carotid artery disease, complicated cataract surgery, trauma, asteroid hyalosis, and uveitis, whereas high myopia, chorioretinal, and optic atrophy are considered “protective” factors.[3],[4] Both factors, ocular ischemia, and presence of diabetes mellitus probably contributed to the development of retinal neovascularization in our patient. However, it is pertinent to note that DR did not develop in the fellow eye.

Ocular ischemia is associated with iris or angle neovascularization, which was not seen in our patient.[5] FFA in our patient also did not show any gross increase in arm to retina time on the left side. When ocular ischemia is suspected, but carotid doppler is within normal limits, Doppler imaging of retrobulbar vessels, especially of the ophthalmic artery, should be performed. Doppler ultrasound findings of an increased resistivity index in the ophthalmic artery and central retinal vein may indicate disturbances in the retinal and choroidal circulation in patients with diabetes and can be one of the early changes in DR.[6]


  Conclusion Top


We propose that the slow flow in the ophthalmic artery could have been initially responsible for the NI-CRVO and the later development of DR and PDR in the involved eye. This indicates a need for close follow-up in diabetics with apparent resolution of CRVO.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hayreh SS, Zimmerman MB. Ocular neovascularization associated with central and hemicentral retinal vein occlusion. Retina 2012;32:1553-65.  Back to cited text no. 1
    
2.
Hayreh SS, Zimmerman MB. Fundus changes in central retinal vein occlusion. Retina 2015;35:29-42.  Back to cited text no. 2
    
3.
Duker JS, Brown GC, Bosley TM, Colt CA, Reber R. Asymmetric proliferative diabetic retinopathy and carotid artery disease. Ophthalmology 1990;97:869-74.  Back to cited text no. 3
    
4.
Valone J, McMeel J, Franks E. Unilateral proliferative diabetic retinopathy. II. Clinical course. Arch Ophthalmol 1981;99:1362-6.  Back to cited text no. 4
    
5.
Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology 1997;104:859-64.  Back to cited text no. 5
    
6.
Karami M, Janghorbani M, Dehghani A, Khaksar K, Kaviani A. Orbital Doppler evaluation of blood flow velocities in patients with diabetic retinopathy. Rev Diabet Stud 2012;9:104-11.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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