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Year : 2023  |  Volume : 5  |  Issue : 1  |  Page : 6

A rare case of unilateral traumatic peripheral retinal arteriolar occlusions and neovascularization of optic disc

1 Department of Medical Retina, Uvea and Comprehensive Ophthalmology, Narayana Nethralaya, Bannerghatta Road, Bengaluru, India
2 Department of Uveits and Ocular Immunology, Narayana Nethralaya, Rajajinagar and Bannerghatta Road, Bengaluru, India
3 Department of Glaucoma, Narayana Nethralaya, Bannerghatta Road, Bengaluru, India
4 Department of Retina, Narayana Nethralaya, Bannerghatta Road, Bengaluru, India

Date of Submission07-Sep-2022
Date of Acceptance20-Sep-2022
Date of Web Publication27-Mar-2023

Correspondence Address:
Srilakshmi Srinivasan
Swasthya Eye Care, Anekal Bhannerghatta Road, Bengaluru - 560 076, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pajo.pajo_48_22

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A young adult Asian Indian male presented to us with a 1-month history of trauma to the right eye (RE) with a tennis ball. He had intraocular pressure (IOP) of 32 mmHg while on three topical antiglaucoma drugs and oral acetazolamide, with uncontrolled inflammation in the anterior chamber (AC) and arteriolar occlusions in the periphery. His best corrected visual acuity was 20/20 in RE. Fluorescein angiography of the RE showed the presence of neovascularization of disc (NVD). Magnetic resonance angiography of the head and neck, and blood investigations ruled out the embolic origin of arteriolar occlusion and systemic causes for inflammation. Intra ocular pressure (IOP) and inflammation were controlled with appropriate treatment. NVD resolved with photocoagulation treatment (PRP) for capillary non-perfusion areas in 4 weeks. This case documents the occurrence of arteriolar occlusion, with neovascularization after arteriolar occlusion post blunt trauma, and successful adjunct use of topical cyclosporine in the management of AC inflammation and high IOP.

Keywords: Blunt trauma, cyclosporine in inflammation, neovascularization in trauma, traumatic arteriolar occlusion

How to cite this article:
Srinivasan S, Sanjay S, Rao HL, Subashchandra D. A rare case of unilateral traumatic peripheral retinal arteriolar occlusions and neovascularization of optic disc. Pan Am J Ophthalmol 2023;5:6

How to cite this URL:
Srinivasan S, Sanjay S, Rao HL, Subashchandra D. A rare case of unilateral traumatic peripheral retinal arteriolar occlusions and neovascularization of optic disc. Pan Am J Ophthalmol [serial online] 2023 [cited 2023 Jun 3];5:6. Available from: https://www.thepajo.org/text.asp?2023/5/1/6/372589

  Introduction Top

Blunt trauma to the eye is associated with injuries to different parts of the eye and therefore presents several challenges in management.[1],[2] Severe anterior chamber (AC) inflammation and uncontrolled high intraocular pressure (IOP) due to trauma by themselves are challenging situations to manage. The presence of rare or hitherto unknown features of blunt trauma can further complicate the management.

Hereby, we present a rare case of blunt trauma to the right eye (RE) with peripheral retinal arteriolar blockages associated with neovascularization of disc (NVD), persistent anterior segment inflammation, and high IOP and its successful outcome following treatment.

  Case Report Top

A 27-year-old Asian Indian male presented with a 1-month history of trauma to the RE with a tennis ball. At presentation, he was on the following medications: antibiotic-steroid combination drops four times a day, alpha agonist (AA) thrice a day, beta-blocker (BB) twice a day, carbonic anhydrase inhibitor (CAI) twice a day, and oral acetazolamide 250 mg four times a day, oral prednisolone acetate 40 mg/day, and oral omeprazole 20 mg/day. His best corrected visual acuity was 20/20 in the RE and 20/60 with no improvement with a pinhole in the left eye (LE). RE findings included circumcorneal congestion, pigment deposits on endothelium, the flare of 4+, and cells 4+ in the anterior chamber (AC) (both white and pigmented cells were present). Intra ocular pressure (IOP) by applanation tonometry was 32 mmHg. Gonioscopy of the RE showed open angles with angle recession in <90° and microhyphema. Pigment deposits were present on the anterior lens capsule lens was otherwise clear. Vitreous showed minimal haze and 1+ pigmented cells. Optic disc showed cup to disc ratio of 0.7 with thinning of superior and inferior rims, retina showed multiple pre-retinal hemorrhages (PRH) and occluded arterioles in the periphery in all the quadrants [Figure 1]. Macula was normal.
Figure 1: Fundus photograph (montage) showing occluded peripheral arterioles (arrow heads), multiple pre retinal hemorrhages (Bent arrows), single large pre retinal hemorrhage with a subretinal component (Black arrow)

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He had anisometric amblyopia in LE. Examination of the LE was otherwise normal. Patient's steroid regimen was changed to prednisolone eye drops second hourly to control the inflammation. Topical prostaglandin analogue (PGA) once at night was started as a last resort to medically control the IOP. Two weeks later, AC flare reduced to 2+ and cells to 2+. However, IOP was still 35 mmHg. Topical cyclosporine 0.05% twice daily was added and prednisolone eye drops were reduced to four times/day and oral steroids were tapered by 10 mg/week in an attempt to address steroid response. Fundus examination showed faint NVD along with new pre- and subretinal hemorrhages in the inferior quadrant of RE. Fluorescein angiography (FFA) confirmed the presence of NVD [Figure 2]. Indocyanine green angiography (ICG) did not show choroidal ischemia. FFA and ICG of the LE were normal. Complete blood count, erythrocyte sedimentation rate, serum angiotensin-converting enzyme, peripheral blood smear, lipid profile, HIV, Treponema Pallidum Haemagglutination (TPHA), serum homocysteine levels, and chest X-ray were all normal except for mild neutrophilic leukocytosis. Magnetic resonance angiography (MRA) of bilateral carotids was normal. Pan retinal photocoagulation (PRP) was performed to the capillary nonperfusion areas. Six weeks after presenting to us, IOP in the RE was 14 mm Hg. AC showed no cells/flare, and NVD and PRH had resolved. The patient was maintained on topical cyclosporine 0.05% twice a day (BD), CAI twice a day, BB twice a day, AA thrice a day, and PGA once at bedtime. Oral and topical steroids were completely withdrawn after 2 months.
Figure 2: Fluorescein angiography (montage) in arteriovenous phase showing faint leak at the disc indicating neovascularization. Areas of blocked fluorescence corresponding to areas of PRH (black arrows). Periphery shows occluded arterioles and capillary non-perfusion areas in all quadrants (area outside of the black line). FFA shows no leak along the occluded vessels or in the capillary non-perfusion areas indicating absence of inflammatory cause for the occlusion. No NVE was seen. FFA: Fluorescein angiography, PRH: Pre retinal hemorrhage, NVD: Neovascularization of disc

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  Discussion Top

This case documents traumatic peripheral arteriolar occlusion and its complication, neovascularization at disc. The use of cyclosporine as an adjunctive drug to control the AC inflammation in steroid responders is also demonstrated.

Arteriolar occlusions are common in vascular and inflammatory diseases of the eye. Blunt trauma of the eye is associated with multiple complications including blindness but arterial occlusions are rarely seen.[1],[2] Arteriolar occlusions when seen in blunt trauma most often are central retinal artery occlusions[3] and are associated with traumatic optic neuropathy.[3] Dalma-Weiszhausz et al.[4] report three cases which are the only series with peripheral arteriolar occlusion and note that this could be underreported as it does not cause visual impairment as opposed to macular branch occlusion. They propose that the endothelial damage due to acute stretching of intima facilitated by vasospasm as a response to trauma as the precipitating factor for thrombus formation and occlusion. We postulate this as a probable cause for arteriolar occlusion in our case too. Cases in series by Dalma-Weiszhausz et al.[4] showed arteriolar occlusion in 1–2 quadrants, but in our case, arteriolar occlusion was seen in all quadrants and also developed NVD. Blood investigations and MRA of the head and eye ruled out the possibility of an embolic or inflammatory cause for arteriolar occlusion in our case, pointing toward trauma as the possible cause.

Embolism is the most common cause for retinal arteriolar occlusion. Neovascularization is not seen in arteriolar occlusion as there is acute retinal ischemia and infarction which does not lead to the production of vascular endothelial growth factor (VEGF).[5] In our case, arteriolar occlusion was possibly caused by thrombosis. This could have caused a more gradual and relatively incomplete occlusion increasing the amount of VEGF causing neovascularization.

Cyclosporine A, a selective inhibitor of T lymphocytes, is used as a topical agent predominantly in the management of ocular surface diseases.[6] It has been used as a steroid-sparing agent in steroid-induced glaucoma. Penetration of cyclosporine into the AC is poor[6],[7] which limits its utility in the management of anterior uveitis. Prabhu et al.[7] have suggested that the cornea and ciliary body could act as a reservoir for cyclosporine which helps in the reduction of number of recurrences of anterior uveitis in their case series. In our case, the patient was on four topical and one systemic medication for persistent high IOP. Steroid response was thought as a possible cause for high IOP in this case. Hence, we tried reducing the topical and oral steroids and adding cyclosporine. The addition of cyclosporine reduced the inflammation gradually over a period of 1 month which allowed us to reduce the topical steroids.

  Conclusion Top

Peripheral arteriolar occlusions can occur due to blunt trauma and they may pose a risk of neovascularization at the disc. Topical cyclosporine can be an option when faced with the challenge of AC inflammation and high IOP due to steroid response.

Declaration of patient consent

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

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Eagling EM. Ocular damage after blunt trauma to the eye. Its relationship to the nature of the injury. Br J Ophthalmol 1974;58:126-40.  Back to cited text no. 1
Girkin CA, McGwin G Jr., Long C, Morris R, Kuhn F. Glaucoma after ocular contusion: A cohort study of the United States Eye injury registry. J Glaucoma 2005;14:470-3.  Back to cited text no. 2
Zvorničanin J, Kuhn F, Halilbašić M, Mušanović Z. Central retinal artery occlusion and traumatic optic neuropathy following blunt ocular trauma. Int J Ophthalmol 2018;11:893-7.  Back to cited text no. 3
Dalma-Weiszhausz J, Meza-de Regil A, Martínez-Jardón S, Oliver-Fernández K. Retinal vascular occlusion following ocular contusion. Graefes Arch Clin Exp Ophthalmol 2005;243:406-9.  Back to cited text no. 4
Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: Associated systemic and ophthalmic abnormalities. Ophthalmology 2009;116:1928-36.  Back to cited text no. 5
Perry HD, Donnenfeld ED, Acheampong A, Kanellopoulos AJ, Sforza PD, D'Aversa G, et al. Topical cyclosporine a in the management of postkeratoplasty glaucoma and corticosteroid-induced ocular hypertension (CIOH) and the penetration of topical 0.5% cyclosporine A into the cornea and anterior chamber. CLAO J 1998;24:159-65.  Back to cited text no. 6
Prabhu SS, Shtein RM, Michelotti MM, Cooney TM. Topical cyclosporine a 0.05% for recurrent anterior uveitis. Br J Ophthalmol 2016;100:345-7.  Back to cited text no. 7


  [Figure 1], [Figure 2]


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